editorial desk 1-2 case report basloid ameloblastoma: … · 2017-12-16 · of all oral and...

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1. EDITORIAL DESK 1-2

CASE REPORT

1. BASLOID AMELOBLASTOMA: A RARE ENTITY Gurdeep Singh, Rajkumari Gupta, Abhishek Singhvi

3-7

2. MANAGEMENT OF ERUPTION CYST IN PEDIATRIC PATIENTS Radha Nerkar, Vikram Singh, Rahul Choudhary, Prajakta Joshi

8-12

3. LASER ASSISTED EXCISION OF PYOGENIC GRANULOMA Vandana Sharma, Zoya Chowdhary , Rohit Rai

13-18

4. CRANIO-FACIAL FORM OF POLYOSTOTIC FIBROUS DYSPLASIA Vipul Udawat, Ankita Bohra, Anita B., Sugandha Arya

19-29

5. GROPER’S APPLIANCE: AN ANTERIOR FIXED AESTHETIC APPLIANCE Varsha Parihar ,Rahul Choudhary, Vikram Singh,Pavni Chouhan

30-36

REVIEW ARTICLE

1. A COMPENDIUM ON CELLULAR CANNIBALISM Ripon Chaudhary, Sanya Bhatia

37-42

2. PHOTOACOUSTIC ENDODONTICS USING PIPS™ Raj Rathore, Deepshikha Rathore, Usha Dabas, Vipin K. Dabas

43-48

3. TISSUE ENGINEERING: A REVOLUTION IN BIOLOGIC ERA Pavni Chauhan , Rahul Choudhary, Vikram singh, Varsha Parihar

49-62

4. THE SELF ADJUSTING FILES: A STEP CLOSER TOWARDS PERFECTION Pravek Khetani , Usha Dabas, Vipin K. Dabas

63-68

5. CESSATION: AN ESSENTIAL COMPONENT FOR GLOBAL PUBLIC HEALTH - A REVIEW Sweta Soni

69-81

6. MINIMAL INVASIVE DENTISTRY : A REVIEW Vanisha Mehta, Vikram Singh , Rahul Choudhary, Prajakta Joshi

82-90

7. KEEP CARIES AWAY: GET IMMUNIZED Prajakta Joshi, Vikram Singh, Rahul Choudhary, Vanisha Mehta

91-104

2DENTAL IMPACT vol. 7, Issue 1, June 2015

FROM THE EDITORS DESK: Dear Readers,

With this issue of our journal we are proving that dental science is a fast

Changing field where innovations are the order of the day. The issue has been

Presented with good quality articles of varying nature that have come from Faculties of

other colleges and different states also. would like to thank all of them for their

contribution and support towards this issue of our journal and hope that it will continue

in the forthcoming issues also.This will help the students and professionals to achieve

valuable information Regarding research work and clinical experiences.

Best Wishes

Dr. Raghavendra Kurdekar Professor & Dean

Vyas Dental College & Hospital

3

CASE REPORT

DENTAL IMPACT vol. 7, Issue 1, June 2015

BASLOID AMELOBLASTOMA: A RARE ENTITY

Dr Gurdeep Singh1, Dr Rajkumari Gupta

1, Dr Abhishek Singhvi

2

1Post Graduate Student,

2Reader

Department Of Oral Maxillofacial Pathology , Vyas Dental College and Hospital, Pali road, Jodhpur,

Rajasthan, India

INTRODUCTION:

Ameloblastoma is the most common

odontogenic tumor of the jaw arising from

rest of dental lamina, developing enamel

organ, lining of an odontogenic cyst or

from basal cells of oral mucosa. It is the

most common odontogenic tumor of jaw,

second to Odontomas. Ameloblastoma is

slow growing, locally invasive tumor that

runs a benign course in most cases.[1]

Histoloical variants of ameloblastoma are

follicular, plexiform, desmoplastic, basal

cell, acanthomatus and granular cell.

Prevalence of odontogenic tumor is 0.8%

of all oral and maxillofacial pathology.

30% of all odontogenic tumors are

contributates by ameloblastoma making it

a most common tumor of odontogenic

origin.[2] Molar region and ascending

ramus are the common site of occurrence

in mandible and only few cases occurs in

maxillary region.[3] Despite their

destructive nature they are considered as

benign.[4] The basal cell variant of

ameloblastoma are limited and majority of

the cases have been reported to occur in

the mandible.[5] Resmblence of

microscopic features of basal cell

ameloblastoma, with malignant tumors,

like basaloid squamous cell carcinoma,

cutaneous basal cell carcinoma and solid

ABSTRACT:

Ameloblastoma is relatively most common epithelial odontogenic tumor of jaws

with high rate of reccurence, which includes several histological variants like

follicular, plexiform, desmoplastic, basal cell, acanthomatus and granular cell. Basal

cell ameloblastoma is a rarest entity till date, only few cases of basal cell

ameloblastoma have been reported in the literature. Considering the rarity of the

lesion, we report here an interesting and unique case of basal cell ameloblastoma of

the mandible occurring in a 24 year old female patient.

KEY WORDS: Ameloblastom, Basal cell, Odontogenic tumor.

4

BASLOID AMELOBLASTOMA: A RARE ENTITY Singh G et al


type adenoid cystic carcinoma, may

sometimes fails pathologist to

differentiate it from intraoral basaloid

squamous cell carcinoma leading to

erroneous diagnosis.[6] Here we describe a

rare case of ameloblastoma in a 24 yearr

old female with detailed clinical,

radiographic and histopathological features

suggesting it to be a ameloblastona with

basal cell variant.

CASE REPORT:

A 24 year old female patient complained

of painless swelling in relation to left

lower mandibular posterior region. Past

medical, dental and family history of the

patient was unremarkable. There was no

history of trauma or pus discharge. Extra

oral examination revealed facial

asymmetry due to swelling on the left side

of the face extending antero-posteriorly

from corner of mouth to angle of mandible

and supero-inferiorly involving zygomatic

area and border of mandible (Figure 1).

Clinical examination revealed swelling

was soft in consistency, afebrile, and

fluctuant with normal overlying skin. Left

Submandibular lymph node was palpable

and non tender.

Intra oral examination revealed swelling in

left mandibular third molar 38 (FDI 38)

was present which was soft to firm in

consistency and caused buccal cortical

plate expansion, 3X2 cm in its greatest

dimension. Anterio-posteriorly swelling

extends from distal surface of 38 to ramus

of mandible. Overlying mucosa was pink

in color. OPG revealed expansile,

multilocular radiolucency involving

coronoid process, ramus, angle of

mandible extending up to apices of 38,

however mandible continuity in the lower

border and posterior border of left side

seems to be intact (Figure 2).

An incisional biopsy of the lesion was

performed, and the specimen was referred

for histopathological evaluation. On

macroscopic examination 1 bit of soft

tissue was received for histopathological

diagnosis. Tissue was firm in consistency,

creamish brown in color with irregular

margins, measuring 3X2 cm. Microscopic

examination revealed lesional tissue

composed of nest of uniform basaloid

cells, the peripheral cells were cuboidal to

short columnar with reversal of polarity.

Occasional mitosis was evident along with

palisading appearance of nuclei. Based on

the available supporting evidence final

diagnosis of basal cell ameloblastoma was

given. In this case hemi mandibulectomy

was performed under general anaesthesia.

5



Figure 1: Facial Asymmetry On Left Side

From Corner Of Mouth To Lower Angle

Of Mandible.

Figure 2: OPG Revealed Expansile,

Multilocular Radiolucency Involving

Ramus, Angle Of Mandible Extending Up

To Apices Of Mandibular 3rd

Molar,

However Mandibular Continuity In The

Lower Border & Posterior Border Of Left

Side Seems To Be Intac

Figure 3:Stratified Squamous Epithelium

Covering Loose CT Stroma. The CT

Shows Numerous Islands And Nests Of

Basaloid Epithelial Cells With Peripheral

Cuboidal Cells.

DISCUSSION:

Odontogenic tumors are the lesions

originating from epithelial and/or

mesenchymal components of the tooth

forming apparatus. They are unique and if

left untreated often lead to extensive tissue

destruction. Ameloblastoma is the most

frequent and enigmatic odontogenic tumor.

The term ameloblastoma has been derived

from Old French, amel – enamel, plus

Greek word blastoma meaning germ and

“adamantinoma” greek word adamos

meaning hard substance.[7]

Ameloblastoma is a rare benign

odontogenic tumor, it affects either gender

and can occur at any age, 50% occur

between age 20 to 30 years. Adebiyi et al

clincopathologically analyzed the

histological variants of ameloblastoma and

observed the basal cell variant of

6



ameloblastoma occurs in mandible region

of males with 30-40 years age as common

age of occurrence. The occurrence in the

mandible is 5 times higher than in the

maxilla.[8] In the article we are presenting

a case of 23 year old female with

mandibular site which is similar with the

data as given in literature.

The basal cell variant of ameloblastoma is

rare a variant.[9,10] Basal cell

ameloblastoma tends to grow in an island

like pattern, basaloid appearing cell tend to

stain deeply basophilic. The cells in the

central portion may be polyhedral, but no

stellate reticulum like cells are seen. The

peripheral cells tend to be low columnar to

cuboidal and usually do not demonstrate

reverse of polarity nuclei. However,

hyperchromatism and palisading of the

nuclei normally are retained.[11] The

islands of uniform baseloid cells in a

mature fibrous connective tissue stroma

are seen.[12] Our histological findings in

the present case were in unison with the

above described features. Basal cell

ameloblastoma shows remarkable

resemblance to basal cell carcinoma.

Hence distinction between these two

lesions is of paramount importance.

Progonosis of basal cell type of

ameloblastoma is very difficult to predict

as only limited number of cases have been

reported so far.[6]

The surgical resection

of the tumor remains the mainstay

treatment modality. The maxillary lesions

needs to be treated more aggressively due

to potential spread to vital structure.[5]

However some authors favor conservative

treatment as they believe that

ameloblastoma though benign in nature

should be treated by conservative approach

because of serious cosmetic, functional

and reconstructive problems with it.

CONCLUSION:

The frequency of ameloblastoma and its

persistent growth causing facial

asymmetry requires it to be diagnosed

accurately followed by adequate

management. Basal cell variant like

reported in the article needs appropriate

diagnosis based not only on clinical and

radiologic principles but also on sound

histopathologic analysis. Long-term

follow-up at regular intervals of this

aggressive variant is necessary to establish

the recurrence rate.

REFRENCES:

1. Giraddi GB, Bimleshwar, Singh C

et al. Ameloblastoma – Series of 7

treated cases- and review of

literature. Arc Oral Sci

Res.2011;1:152-5.

2. Beena VT, Choudhary K, Heera R

et al. Peripheral Ameloblastoma: A

Administrator

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Administrator

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7



case report and review of literature.

Case Reports Dent.2010;3:1-6.

3. Small IA, Waldron CA.

Ameloblastoma of the jaws. Oal

Surg Oral Med Oral

Pathol.1995;89:457-65.

4. Reddy RS, Ramesh T, Laxmi V et

al. Desmoplastic Ameloblastoma-

A distinct clinco-pathology entity.

Int J Dent Case Reports.2011;1:52-

60.

5. Giraddi GB, Anusha AJS. Basal

cell Ameloblastoma- Review of

literature with report of three cases.

J Oral Biol Cranifac

Res.2012;2:53-6.

6. Sridhar M, Rddy LRB, Kharat S et

al. Basal Cell Ameloblastoma: A

rare histological variant of an

uncommon tumor. Nier J

Sur.2015;21:66-9.

7. Lamsoe TR, Jayakumar K, Michael

MJ. Hybrid Ameloblastoma

(granular cell variant): A case

report. Int J Case Report

Images.2013;4:1-6.

8. Saify F, Sharma N. Basal cell

ameloblastoma: A rare case report

and review of literature. Oral

Maxillofac Pathol J. 2010;1:1–7.

9. Neville, Damm, Allen et al. Oral

and maxillofacial pathology. 3rd

ed.

Elsevier Inc, India.2009.

10. Shafer, Hine, Levy. Text book of

oral Pathology.7th

ed. Elsevier Inc,

India.2012.

11. Kessler HP. Intraosseous

ameloblastoma. Oral Maxillofac

Surg Clin North Am. 2004;

16:309-22.

12. Shakya H, Khare V, Pradhe N.

Basal cell ameloblastoma of

mandible: A rare case report with

review. Case Reports Dent.

2013;1:1-6.

Administrator

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CASE REPORT


MANAGEMENT OF ERUPTION CYST IN PEDIATRIC PATIENTS

Dr. Radha Nerkar1, Dr. Vikram Singh

2, Dr.Rahul Choudhary

2, Dr. Prajakta Joshi

1


2Senior Lecturer

Department Of Pedodontics, Vyas Dental College and Hospital, Pali road, Jodhpur, Rajasthan, India

INTRODUCTION:

An eruption cyst (EC) ususlly occurs in the

soft tissues and is an essence a dentigerous

cyst (DC). The dentigerous cyst develops

around the crown of an unerupted tooth

lying in the bone, whereas the eruption cyst

occurs when a tooth is impeded in its

eruption within the soft tissues overlying the

bone.[1] The eruption cyst is a form of soft

tissue benign cyst accompanying an erupting

primary or permanent teeth and happens to

appear shortly before appearance of these

teeth in the oral cavity.[2] The cyst results

from a separation of the dental follicle from

the crown of an erupting tooth and fluid

accumulation occurs within this created

follicular space. Most authors refer to EC as

a cystic lesion, which is not similar to DC.

According to the World Health Organization

(WHO) classification of epithelial cysts of

the jaws, EC is a separate entity.[3]

CASE REPORT:

A 7 years old girl reported to the dental

outpatient department with a complaint of

swelling on the upper right back teeth region

since 3 months. Clinical examination

revealed a 3x3 cm dome shaped raised

swelling in the region of maxillary right

deciduous second molar region, which was

pale pink in color ,asymptomatic, except the

appearance(Figure 1). Based on the history

ABSTRACT:

Eruption cyst is a benign cyst associated with a primary or permanent tooth in its

soft tissue phase after erupting through the bone. It is the soft tissue analogue of the

dentigerous cyst, but recognized as a separate clinical entity .It is clinically

significant in that knowledge among general dentists is very essential regarding this

developmental disturbance to reach the correct diagnosis and to provide proper

treatment. We are reporting a case of eruption cyst in an 7 year old girl.

KEY WORDS: Eruption cyst, primary teeth ,soft tissue, benign.

9

ERUPTION CYST: A CASE REPORT Nerkar R et al


and clinical findings a diagnosis of eruption

cyst was made. Surgical exposure was

carried out to expose the erupting

tooth(Figure 2).

The specimen send for histopathological

examination showed surface oral epithelium

on superior aspect, underlying lamina

propria showed variable inflammatory cell

infiltrate(Figure 3). The roof of the cyst

showed thin layer of non keratinizing

squamous epithelium. The diagnosis of

eruption cyst was confirmed.

Figure 1:Solitary Nodule On Gingiva in

relation to 55

Figure 2:Surgical Exposure At The Site Of

Lesion

Figure 3: Excised Tissue After Removal Of

Lesion

DISCUSSION:

The etiology of EC is controversial. Some

researchers have attributed its development

to degenerative cystic changes in the

reduced enamel epithelium following

completion of amelogenesis, while others

suggest that the cyst develops from the

10



epithelial remnants of the dental lamina

overlying the eruption tooth. The pathology

behind EC is probably similar to that of DC.

The difference is that, in EC, the tooth is

hampered in breaking through to the surface

by the soft tissues of the gingival rather than

the bone.[4] These cysts are usually found

in children of different ages, and

occasionally in adults if there is delayed

eruption.[1] These cysts are have low

prevelance. This may be due to the fact that

many authors classify them under the

dentigerous cyst and since they are benign,

the definitive diagnosis has been done in

very few studies by the authors.[5] The cysts

are found in children of different ages, and

occasionally in adults if there is delayed

eruption. In a series of 27 patients with 36

eruption cysts reported by Aguilo et al.

(1998), the lesions occurred within an age

range of 5–9years; while in the study of 24

patients reported by Bodner et al. (2004).[1]

Clinically , the appearance of eruption cyst

is like that of dome shaped raised swelling

in the mucosa of the alveolar ridge, which is

soft to touch and color varies from

transparent, bluish purple to blue black.[6]

However it may be either the colour of

normal gingiva or blue. It is usually painless

unless infected and is soft and fluctuant1

.

Approximately it measures about 6mm in

diameter.[7] However the size depends on

whether it is associated with primary or

permanent teeth involved.[6] In most of the

cases eruption cysts are found to be

asymptomatic but there can be pain on

palpation due to secondary factors such as

trauma or infection. Differential diagnosis

should be considered before delivering any

treatment and varies from granuloma,

amalgam tattoo and Bohn,s nodule to

eruption hematoma.[5] The eruption

hematoma occurs because of bleeding from

the gingival tissue during eruption and the

collection of blood is external to the

epithelium of the enamel.[8] The exact

etiology of occurrence of eruption cyst is not

clear. Aguilo et al, in their retrospective

clinical study of 36 cases, found early caries,

trauma, infection and the deficient space for

eruption as possible causative factors.[5]

Most of the time eruption cyst occurs as an

isolated phenomenon , although a case has

been reported showing other associated

anomalies like hamartomas, natal tooth and

epstein pearls in a premature newborn

baby.[9] Sometimes EC may be associated

to natal or neonatal teeth .It has been

classified as mature natal or neonatal when

the tooth is nearly or fully developed and

has relatively good prognosis for

maintenance, and immature natal or neonatal

11



when the tooth has incomplete or

substandard structure, implying in poor

prognosis. Removal of natal or neonatal

teeth is suggested when they interfere with

feeding, have highly mobility, and/or are

poorly developed.[10] Mostly, the eruption

cysts does not require treatment and most of

them disappear on their own. When they

hurt, bleed, are infected, or esthetic

problems arise, surgical intervention is

required.[6] Interventional treatment may

not be necessary because the cyst ruptures

spontaneously, thus permitting the tooth to

erupt.[8] These cysts are most frequently

treated by marsupialisation, but in the series

of 24 cases reported by Bodner et al (2004),

12 were treated by marsupialisation, 10

resolved without treatment, and in two cases

the involved teeth were extracted. The dome

of the cyst is excised, exposing the crown of

the tooth which is allowed to erupt.[1] Use

of Er, Cr-YSGG laser for treatment of

eruption cysts is suggested by Boj et al. It

has certain advantages over conventional

exposure with scalpel. They can be listed as

non-requirement of anesthesia, no excessive

operative bleeding, does not produce heat or

friction and patient will be

comfortable.[5,7,11]

REFRENCES

1. Shear M, Speight P. Cysts of the Oral and

Maxillofacial Regions. Fourth

edition,1996,99-102.

2. Anderson RA. Eruption cysts: A

retrograde study. J Dent Child 1990;57:124-

7.

3. Bodner L, Goldstein J, Sarnat H. Eruption

cysts: A clinical report of 24 new cases. J

Clin Pediatr Dent 2004;28:183-6.

4. Woldenberg Y, Goldstein J, Bodner L.

Eruption cyst in the adult-a case report. Int J

Oral Maxillofac Surg 2004;33:804-5

5. Aguilo L, Cibrian R, Bagan JV, Gandia

JL. Eruption cysts: Retrospective clinical

study of 36 cases. J Dent Child

1998;65:102-6.

6. Nagaveni NB, Umashankara KV,

Radhika NB, Maj Satisha TS. Eruption cyst:

A literature review and four case reports.

Indian J Dent Res 2011;22:148-51.

7. Seward M. Eruption cyst: An analysis of

its clinical features. J Oral Surg 1973;31:31-

5.

8. Bodner L. Cystic lesions of the jaws in

children. Int J Pediatr Otorhinolaryngol

2002; 62:25-9.

12



9. Hayes PA. Hamartomas, eruption cyst,

natal tooth and Epstein pearls in a newborn.

ASDC J Dent Child 2000;67:365-8.

10. Rao RS, Mathad SV. Natal teeth: Case

report and review of literature. J Oral

Maxillofac Pathol 2009;13:41-6.

11. Ricci HA, Parisotto TM, Giro EM, de

Souza Costa CA, Hebling J. Eruption cysts

in the neonate. J Clin Pediatr Dent

2008;32:243-6.

13

CASE REPORT


LASER Assisted Excision of Pyogenic Granuloma: A Case Report

Dr. Vandana Sharma1, Dr.Zoya Chowdhary

2 , Dr. Rohit Rai

3

1Senior lecturer, Vyas dental college and hospital, Jodhpur,

2Post graduate, Teerthanker Mahaveer dental

college and research centre, Moradabad, 3Senior lecturer, Dental College and hospital, Azamgarh

Department Of Periodontics, Vyas Dental College and Hospital, Pali road, Jodhpur, Rajasthan, India

INTRODUCTION:

Pyogenic granuloma (PG) is a hyperactive

benign inflammatory lesion commonly seen

in the oral cavity with gingiva being the

most common affected site followed by

buccal mucosa, tongue and lips. The first

case of PG described in English literature

was in 1844 by Hullihen [1], Later in 1897,

it was described as “botryomycosis

hominis”[2]. In 1904, Hartzell [3] gave the

current term of “pyogenic granuloma” or

“granuloma pyogenicum”. Angelopoulos [4]

histologically described it as

“hemangiomatous granuloma” due to the

presence of numerous blood vessels and the

inflammatory nature of the lesion. The name

for PG is misleading because it is not a true

granuloma. In actuality, it is a capillary

hemangioma.[5,6] It is known by a variety

of names such as Crocker and Hartzell’s

disease, granuloma pyogenicum, granuloma

pediculatum benignum, benign vascular

tumor and during pregnancy as granuloma

gravidarum.

ABSTRACT:

Pyogenic granuloma is a commonly occurring inflammatory hyperplasia of the skin

and oral mucosa. It is a tumor-like growth of the oral cavity, which usually arises

due to physical trauma or hormonal factors & irritation. Clinically oral pyogenic

granuloma is seen as a smooth exophytic lesion with usually haemorrhagic base.

The peak prevalence is in teenagers and young adults, but it may occur in any age

group especially in individuals with poor oral hygiene. Females are far more

susceptible than males because of the hormonal changes that occur during

pregnancy, puberty and menopause. The treatment is excision of the lesion in toto.

This paper presents a case of pyogenic granuloma managed by use of laser

intervention.

KEY WORDS: Benign lesions, Granuloma, Hyperplasia, Pyogenic granuloma.

14

LASER Assisted Excision of Pyogenic Granuloma: A Case Report Sharma V et al


The lesion usually arises in response to

various stimuli such as low-grade local

irritation, traumatic injury, hormonal factors,

or certain kinds of drugs.[7] Pyogenic

granuloma may occur in all age groups,

though it is predominantly seen in females

because of the hormonal changes that occur

in women during puberty, pregnancy, and

menopause. Some of the lesions regress on

its own after the birth of the child. But in

many cases, mastication on the lesion causes

bleeding and pain and requires surgical

intervention. Treatment of pyogenic

granuloma involves a complete surgical

excision. Recurrence of pyogenic granuloma

after excision is known to be 16% and so re

excision of such lesions might be necessary.

Being a non-neoplastic growth, excisional

therapy is the treatment of choice but some

alternative approaches such as cryosurgery,

excision by Nd:YAG Laser, flash lamp

pulsed dye Laser, injection of corticosteroid

or ethanol, and sodium tetradecyl sulphate

sclera therapy have been reported to be

effective.[8]

So, this case report explains the use of diode

laser for the management of pyogenic

granuloma.

CASE REPORT:

A 22-year-old female patient reported to the

Department of Periodontology with a

complaint of growth in the upper left front

tooth region since 1year. To start with the

lesion was peanut in size and slowly

progressed to attain the present size (Figure

1). She also complained of the lesion being

associated with bleeding while brushing.

There was no history of swelling in any

other part of the body and had no relevant

medical history.

Extraoral Examination-

No abnormality detected.

Intraoral examination-

Inspection: A solitary gingival over

growth was visible between maxillary

left central incisor and lateral incisor on

labial aspect measuring 1.3x1.7mm in

size. The growth was roughly oval in

shape, color is varying from pinkish red,

and surface was smooth. The oral

hygiene status was found to be poor

(Figure 1).

Palpation: The inspectory findings

regarding number, site, shape and size

were confirmed. The growth was firm on

palpation, non-tender with absence of

discharge. Bleeding on provocation was

positive.

Radiographic findings: Intraoral

periapical radiograph (IOPAR) revealed

no abnormalities (Figure 2).

Blood Examination-

15



Revealed normal values.

Histopatholoigical Examination-

Histopathological examination showed a

hyperplastic, parakeratinized stratified

squamous epithelium. The connective tissue

was loose fibrillar and comprised of

numerous proliferating capillaries, dense

mixed inflammatory infiltrate, and

extravasated red blood cells (Figure 3). The

histopathological examination confirmed the

clinical diagnosis of Pyogenic granuloma.

Treatment-

The treatment comprised of oral prophylaxis

and excisional biopsy of the growth with

diode laser. To start with thorough scaling &

root planning was carried out & the response

to the same was evaluated after 3-4 weeks of

time. Then the excisional biopsy of the

lesion was done by using diode laser

(Figures 4, 5). Following saline & covered

with periodontal dressing (Coe-Pac). Post-

operative instruction were given to the

patient along with prescription of

amoxicillin 500 mg TID, analgesics 500 mg

SOS, chlorhexidine mouth wash, 10 ml

twice a day for 10 days was given. The

patient was recalled after 1 week, the

healing of the site was uneventful (Figure 6)

& the patient was kept under long term

maintenance. After 6 month again the

patient was recalled for follow up, the

healing was focus to be uneventful &

satisfactory without any sign of recurrence.

Figure 1: Pre-operative photograph

Figure 2: Radiographic of the patient

Figure 3: Histologic section of the lesion

Figure 4: After excision

16



Figure 5: Excised tissue

Figure 6: Post-operative after 1 week.

DISCUSSION:

Gingival enlargement is defined as an

increase in size of the gingiva. Depending

on etiologic factors, gingival enlargement

can be of many types like inflammation,

drug induced effects, neoplasm, hormonal

imbalance, non-specific conditioned

enlargement and systemic involvement like

Leukemia, Wegener's granulomatosis etc [7]

Nonspecific conditioned enlargement, or

pyogenic granuloma, is a benign, localized

mass of exuberant granulation tissue. It is

considered as an exaggerated conditioned

response to minor trauma or chronic

irritation.[9] However, the term is a

misnomer since the condition is not

associated with pus formation and does not

represent a granuloma histologically.[10]

Pyogenic granulomas occur at any age, but

they most frequently affect young adults.

The maxillary gingiva (especially in the

anterior region) is involved more frequently

than the mandibular gingiva; the facial

gingiva is involved more than the lingual

gingiva. Three quarters of all oral pyogenic

granulomas occur on the gingiva, with the

lips, tongue (especially the dorsal surface),

and buccal mucosa also affected. A history

of trauma is common in extragingival sites,

whereas most lesions of the gingiva are

response to irritation. Individual’s with poor

oral hygiene and chronic oral irritants most

frequently are affected.[11,12] Early lesions

bleed easily due to extreme vascularity.

Pyogenic granulomas can have a rapid

growth pattern that can cause alarm. If left

alone, a number of pyogenic granulomas

undergo fibrous maturation and resemble

and/or become fibromas.

Histologic examination reveals sectioned

soft tissue consisting of a lesion composed

of ulcerated mucosa covering a core of

cellular fibrous connective tissue admixed

with proliferating vascular channels and a

mixed inflammatory infiltrate. This lesion is

17



a reactive/ inflammatory process.

Differential diagnosis for PG is fibroma,

peripheral ossifying fibroma, irritation

fibroma, peripheral giant cell granuloma.

The treatment of choice is conservative

surgical excision. For gingival lesions,

excising the lesion down to the periosteum

and scaling adjacent teeth to remove any

calculus and plaque that may be a source of

continuing irritation is recommended.[13]

Pyogenic granuloma occasionally recurs,

and a re-excision is necessary. The

prognosis is excellent, and the lesion usually

does not recur unless inadequately removed.

Focus patient education on better oral

hygiene, and consider recommending

pulsating mechanical toothbrushes with

timers. These tooth brushes encourage better

hygiene.[5]

Laser therapy using continuous and pulsed

CO2

and Nd:YAG systems have been used

for a variety of intraoral soft tissue lesions

such as haemangioma, lymphangioma,

squamous papilloma, lichen planus, focal

melanosis, and pyogenic granuloma,

because they carry the advantage of being

less invasive and sutureless procedures that

produce only minimal postoperative pain.

Rapid healing can be observed within a few

days of treatment, and as blood vessels are

sealed, there are both a reduced need for

post-surgical dressings and improved

haemostasis and coagulation. It also

depolarizes nerves, thus reducing post-

operative pain and also destroys many

bacterial and viral colonies that may

potentially cause infection. Reduced post-

operative discomfort, oedema, scarring and

shrinkage have all been associated with its

use.[4]

CONCLUSION:

Pyogenic granuloma is a common lesion of

the skin and oral cavity, especially the

gingiva. From the present case report it is

concluded that pyogenic granuloma can be

adequately treated with the correct diagnosis

and proper treatment planning. A careful

excision of the lesion with Laser is a

successful treatment option and also helps in

preventing the recurrence of the benign

lesion.

REFERENCES:

1. Hullihen SP. Case of aneurism by

anastomosis of the superior maxillae.

Am J Dent Sci. 1844;4:160-2.

2. Bhaskar SN, Jacoway JR. Pyogenic

granuloma – Clinical features,

incidence, histology, and result of

treatment: Report of 242 cases. J

Oral Surg. 1966;24:391-8.

18



3. Hartzell MB. Granuloma

pyogenicum. J Cutan Dis Syph.

1904;22:520-5.

4. Angelopoulos AP. Pyogenic

granuloma of the oral cavity:

Statistical analysis of its clinical

features. J Oral Surg. 1971;29:840-7.

5. Sheiba R Gomes, Quaid J. Shakir,

Prarthana V Thaker, Jamshed K

Tavadia. Pyogenic granuloma of the

gingiva: A misnomer - A case report

and review of literature. J In Soc

Periodontol. 2013;17:514-9.

6. Sanjay, Venugopal, Shobha KS,

Netravathi TD. Pyogenic granuloma

– A case report, J Dent Sci & Res.

1:1:80-5.

7. Sumanth Shivaswamy, Nazia

Siddiqui, A. Sanjay Jain, Ajit Koshy,

Sonal Tambwekar, Akhil Shankar. A

rare case of generalized pyogenic

granuloma: A case report.

Quintessence Int. 2011;42:493–9.

8. Jafarzadeh H, Sanatkhani M,

Mohtasham N. Oral pyogenic

granuloma: A Review. J Oral Sci.

2006;48:167-75.

9. Ningappa Chinnannavar Sangamesh,

Bellguppa Poornima, Kodige

Chandrashekar Vidya, Santosh

Bhopal Sakri. Extragingival

pyogenic granuloma: A rare case

report. Journal of the Scientific

Society 2013;40:49-51.

10. Reet Kamal, Parveen Dahiya,

Abhiney Puri. Oral pyogenic

granuloma: various concepts of

etiopathogenesis. Journal of Oral and

Maxillofac Pathol. 2012;16:79-82.

11. Ramirez. K, Bruce G, Carpenter W.

Pyogenic granuloma: case report in a

9-year-old girl. General Dent.

2002;50:280-1.

12. A Maryam, Farnaz F, Nooshin M,

Pegah Mosannen M. Extragingival

pyogenic granuloma: A Case Report.

Cases Journal. 2008; 1:371.

13. Saikhedkar R, Shrivastava S,

Melkundi M, Viswanathan V.

Pyogenic granuloma – A Case

Report. Int J Dental Clinics.

2011;3:87-8.

30

CASE REPORT


GROPER’S APPLIANCE: AN ANTERIOR FIXED AESTHETIC APPLIANCE

Dr Varsha parihar 1, Dr.Rahul Choudhary

2, Dr. Vikram Singh

2, Dr. Pavni Chouhan

1


2Senior Lecturer


INTRODUCTION

Aesthetic rehabilitation of a preschooler

who has suffered multiple tooth loss

subsequent to early childhood caries (EEC)

or extensive dental trauma is one of the

greatest challenges for pediatric dentist. The

implications of this situation include

decreased masticatory efficacy, speech

disturbances, development of parafunctional

buccal habits.[1]

When extraction of primary incisors is

necessary, many parents will seek an

aesthetic solution to replace the lost front

teeth. For clinician seeking to construct and

place an aesthetic appliance in a young

toddler there is very little information in the

dental literature which addresses indications

ABSTRACT

Aesthetic rehabilitation of a preschooler who lost teeth due to extensive trauma

is common problem faced in pediatric clinic. Restorative option available

includes removable or fixed appliance. This article discusses about simple

technique for placement of fixed type of anterior aesthetic appliance. These

appliances are always considered an elective appliance and their placement is

usually dictated by the wishes of the parent.

KEYWORDS: Aesthetic, appliance, rehabilitation, avulsion.

31

Groper’s appliance: An anterior fixed aesthetic appliance Parihar V et al


or contraindications for these appliances. A

few articles have been published which

describe a particular design for these

appliances.[2,3,4] This paper discusses one

type of anterior fixed aesthetic appliance

that was fabricated to replace the primary

upper two central incisors in a four year old

girl.

CASE REPORT

A four year old girl reported to the

Department of Pedodontics and Preventive

Dentistry, with a chief complaint of missing

upper two central incisors. On examination

51 and 61 were found to be absent (figure1).

An investigation revealed that these teeth

were avulsed during a traumatic fall which

had taken place about 1 year ago. The

parents had not visited a dentist after the

injury and the teeth were never retrieved.

The patient and her parents were concerned

with the deprived anterior aesthetics. It was

decided to make an anterior aesthetic fixed

appliance for replacing the missing anterior

teeth. Maxillary primary second molars (55

and 65) were banded (band size: 0.005” x

0.180”) and alginate impressions were made

for the upper and lower arches.

Contra-indications of these appliances may

include children with seizure disorders,

mental retardation, a poor ability to be

followed-up, poor oral hygiene, immune-

compromised patients, inappropriate oral

habits and deep-bite, over-jet, or anterior

crossbite. However, our patient did not

suffer from any of the above conditions.

Casts were poured with dental stone. On the

upper cast, a stainless steel wire (1.00 mm)

framework was made, spanning from one

band to the other, while making a zig-zag

pattern in the anterior region to reinforce the

acrylic segment. The ends of the wire were

then soldered to the corresponding molar

bands (Figure 2).Teeth were fabricated using

composite A2 shade. A trial wax up was

done (Figure 3). Occlusion is checked with

lower cast. After that cold mould seal is

applied in all the extensions required then

denture base was fabricated using cold cure

acrylic (Figure 4).

The appliance was then removed from the

cast and it was tried intra-orally (Figure 5).

After necessary trimming and polishing, the

appliance was cemented with glass ionomer

luting cement via the molar bands on 55 and

65 (Figure 6).

DISCUSSION

32



The anterior tooth loss results in tipping of

adjacent teeth, over-eruption of opposing

teeth, midline shifting, masticatory

impairment, speech problems and lingual

dysfunction.[5] When considering the need

for an anterior appliance to replace missing

primary incisors few points should be

discussed with the parents. First, is parental

desire.[6] Children who are under fiveyears

of age, with missing anterior teeth, are

seldom affected socially, because of limited

exposure to peers unlike school aged

children. However, children may become

aware of theirappearance when attend

daycare or preschool. As they enter in

school, they will be more comfortable, with

children who actively exfoliate primary

incisors.[7]

For phonations and proper speech lingual

sides of maxillary anterior teeth are needed

by the tongue and absence of these teeth

may result in improper speech.[7,8] It

usually affects sounds like ‘s’, ‘z’ and

‘th’.[9] Gable et al found that there is no

long term effects on speech by early loss of

teeth.[10] Moreover, parents of children

who had their incisors extracted, found no

masticatory or speech difficulties in their

children.[11] Speech problems in children

who are over four years of age is

uncommon and if it occurs, they are usually

compensated and reversible.[6] Our patient

had no complaints with mastication or

speech, but she had complaint with

aesthetics.

This fixed type of appliance has

disadvantages; such as need of the patients’

cooperation and chances of breakage.

Jasmine and Groper documented similar

appliance, in which, plastic teeth were

attached to metal cleats that were soldered to

the palatal wire bar instead of being attached

to acrylic [12], like it was in our design.

Although, that appliance would be superior

in hygiene, due to an improper anterior fit or

reduction of ridge height it may pose the risk

of a gap developing between the teeth and

the alveolus. Although our acrylic flange

design would not pose the same risk, lack of

hygiene under the acrylic flange may result

in mucosal irritation. However, if it happens,

the appliance can be temporarily debanded

until the tissue heals.

33



Figure-1 Pre-Operative Photograph Figure-2 Wire Bending After Soldering

(Missing 51 61) And Teeth Arrangement

Figure-3 Trial Wax Up Figure-4 Fabrication Of Acrylic Plate

Figure-5 The Appliance(Intraoral View) Figure-6 The Appliance (Facial View)

The anterior segment from canine to canine

appears to be stable, Unlike the posterior

segment even after early loss of incisors,

with no net loss of space between the

canines.[7] Moreover, the intercanine

growth between ages of two and four years

34



is minimal (less than 0.5mm) and it is

clinically insignificant.[13] After the

eruption of the first permanent molar

Changes in arch

length with tooth migration generally occur.

At this time, the appliance should be

removed, as it interferes with the eruption of

the central incisors.[6] In a crowded

dentition, if one or more incisors are lost,

there may be some rearrangement of space

between the remaining incisors, but no space

maintenance is required if the loss occurs

after the eruption of the primary maxillary

canines.[14] Although there were no

previous records on whether the patient had

spaced, closed or crowded maxillary anterior

dentition, it was known that her primary

canines had erupted before the avulsion had

occurred.

One of the most valid reasons for replacing

missing incisors is to restore a natural and

pleasing appearance and thus provide an

opportunity for normal psychological

development. The possibilities of caries and

growth interference are two other topics that

should be discussed with parents

considering a maxillary esthetic appliance.

Plaque and food debris accumulation is

increased with the fixed anterior appliance.

Therefore, comprehensive caries prevention

program should be initiated with a frequent

recall schedule.

CONCLUSION

A simple technique for appliance placement

was discussed in this paper. The restoration

of anterior aesthetics and function with this

appliance gave a huge psychological boost

for the child. Oral hygiene instructions were

given to the child and her parents. The child

had been asked to visit the department at 3-

month intervals, in order to monitor issues

with regards to hygiene and eruption of the

permanent first molars.

REFERENCES

1. Ripa L.W. Nursing caries - A

comprehensive review. Pediatr Dent

1988;10: 268- 82.

2. Steffen JM, Miller JB, Johnson R.

An esthetic method of anterior space

maintenance. J Dent Child 1971;

38(3):154-7.

3. Klapper BJ, Strizak-Sherwin R.

Esthetic anterior space maintenance.

Ped Dent 1983;5(2):121-3.

35



4. Jasmin JR, Groper JN. Fabrication

of a more durable fixed anterior

esthetic appliance. J Dent Child

1984;51(2):124-7.

5. Liegeois F, Limme M. Modified

bonded bridge space maintainer. J

ClinPediatr Dent. 1999;23:281-4.

6. Waggoner WF, Kupietzky A.

Anterior esthetic fixed appliances for

the preschooler: considerations and a

technique for placement. Pediatr

Dent. 2001;23:147-50.

7. Christensen JR, Fields HW. Space

maintenance in the primary

dentition. Pediatric Dentistry:

Infancy Through Adolescence.

Pinkham JR ed. 2nd ed.

Philadelphia: W.B. Saunders

Company; 1994:358-63.

8. Riekman GA, E Badrawy HE. Effect

of premature loss of primary

maxillary incisors on speech. Pediatr

Dent. 1985;7:119-22.

9. Fymbo L. The relation of

malocclusion of the teeth to defects

of speech. Arch Speech. 1936;1:204-

16.

10. Gable TO, Kummer AW, Lee L,

Creaghead NA, Moore LJ. Premature

loss of the primary maxillary

incisors: Effects on speech

production. J Dent Child.

1995;62:173-9.

11. Koroluk LD, Riekman GA. Parental

perceptions of the effects of

maxillary incisor extractions in

children with nursing caries. J Dent

Child. 1991;58:233-6.

12. Jasmin JR, Groper JN. Fabrication of

a more durable fixed anterior esthetic

appliance. J Dent Child.

1984;51:124-7.

13. Scures CC. Report of the increase in

bicanine diameter in 2 to 4-year-old

children. J Dent Child. 1967;34:332-

5.

14. Nagan P, Wei SHY. Management of

space in the primary and mixed

dentitions. In Pediatric Dentistry:

Total Patient Care, Wei SHY, ed.

Philadelphia: Lea & Febiger;

1988:462-70.

36



49

REVIEW ARTICLE


TISSUE ENGINEERING: A REVOLUTION IN BIOLOGIC ERA

Pavni Chauhan

1, Rahul Choudhary

2, Vikram singh

2, Varsha Parihar

1.


2Senior Lecturer


INTRODUCTION

The stem cell was proposed by Russian

histologist Alexander Maksimov for

scientific use in 1908.[1,2] Stem cells are

pluripotential cells , can divide and multiply

for an extended period of time,

differentiating into a various specialized cell

types and tissues. Dental stem cells among

adult mesenchymal stem cells, are a subset,

highly proliferative and have the ability to

differentiate into many cell lines.[3] The

most familiar application of adult stem cell

therapyis bone marrow transplantation to

treat metabolic disorders, hematopoietic

cancers and congenital immunodeficiency

syndromes. Stem cell therapy is undergoing

clinical testing for conditions such as

Parkinson’s disease, brain trauma/spinal

cord injuries and diabetes.[4,5] Among

various suggested applications related to

oral health care includes wound healing and

regeneration of dental and periodontal

ABSTRACT:

Stem cells are pluripotential cells which can divide and multiply for an extended

period of time, differentiating into a various specialized tissues and cell types.

Suggested applications related to oral health care have included wound healing and

regeneration of periodontal tissues dental along with craniofacial structures. The

stem cells of dental origin can certainly generate the dental tissues. The growth

factors and the morphogenic factors bind to specific membrane receptors and they

trigger a series of signaling pathways. The stem cells are identified by various

techniques like fluorescence-activated cell sorting, flow cytometry and magnetic-

activated cell sorting and by using biomarkers.

KEY WORDS: Stem cells, Signaling pathways, Cell surface markers,

Developmental Potential.

50

TISSUE ENGINEERING: A REVOLUTION IN BIOLOGIC ERA Chauhan P et al


tissues as well as craniofacial structures

(e.g., repair of cleft lip/palate).[6]

Studies have identified several niches of

multipotent mesenchymal progenitor cells,

known as dental pulp stem cells, which have

a high proliferative potential for self-

renewal. These progenitor stem cells are

now recognized vital to dentine regeneration

process following injury. More recently,

researchers have discovered that stem cells

harvested from deciduous teeth may be a

source of tissue regeneration and repair.[7]

Advances have been made in identifying

dental stem cells and their differentiation

potential. Five different types of dental stem

cells isolated from dental soft tissues are

dental pulp, apical papilla, dental follicle

and periodontal ligament. These cells

express various arrays of biomarkers

including those specific for embryonic

and/or mesenchymal stem cells. In vitro and

in vivo studies have revealed that these stem

cells varied in their differentiation and

proliferation potential.[8]

DENTAL PULP STEM CELLS

These cells were isolated for first time from

permanent third molars by Gronthos et al in

2000. Dr. Songtao Shi a pedodontist,

discovered baby tooth stem cells while he

used the deciduous teeth of his six year old

daughter in 2003 and named those cells as

stem cells from the human exfoliated

deciduous teeth (SHED). Dental Pulp Stem

Cells (DPSCs) can be found within the ‘‘cell

rich zone’’ of the dental pulp. Their

embryonic origin from neural crests,

explains their multipotency. These stem

cells exhibit differentiation potential towards

adipocytes, neurons, chondrocytes and

mesenchymal stem cells.[9,10,11] These are

most potential stem cells which have wide

therapeutic applications.[12] Dental pulp

stem cells can be found both in children and

adults.[13]

Stem cells of dental origin can certainly

generate dental tissues.[14,15,16,17,18] The

SHED and DPSCs are capable of generating

a tissue that has functional and

morphological characteristics that closely

resemble those of the human dental pulp

.[19,20,21,22]

Unlike umbilical cord blood cells which

have to be collected immediately at birth,

the dental stem cells are derived from

deciduous and permanent teeth. There are 20

viable deciduous teeth and 32 permanent

teeth which can be used for collecting stem

cells. This is non-controversial and the stem

cells can be collected without involvement

of any ethical issues. The viable dental stem

51



cells are very simple to collect, without any

mortality and morbidity.[23]

THE DENTAL PULP STEM CELL

DIFFERENTIATION AND THE

SIGNALING MOLECULES

The morphogenic and growth factors bind to

specific membrane receptors and trigger a

series of signaling pathways. These

signaling molecules during the development,

play a major role in cellular functions and

have an important role in the signaling

reparative processes in the dentin and the

pulp.[24,25] When they are released from

the dentin, they are bioactive and fully

capable of inducing the cellular responses,

for e.g., generation of the tertiary dentin and

dental pulp repair.[25,26] The arrangement

of the dentin facilitates the movement of the

growth factors which are released from the

dentin matrix, that are demineralized by

caries, acidic tooth conditioning agents or

pulp capping materials. Calcium hydroxide

has been shown to solubilize dentin and

allow the release of bioactive molecules that

can regenerate dentin.[27] This involves the

recruitment of DPSCs, their differentiation

into odontoblasts, and secretion of

mineralizable matrices.[28,29,30]

THE ISOLATION OF THE DENTAL

PULP STEM CELLS

The stem cells are identified by various

techniques like fluorescence-activated cell

sorting, flow cytometry and magnetic-

activated cell sorting and by using

biomarkers (surface markers and side

populations).[31] Magnetic-Activated Cell

Sorting (MACS) is a method used for the

separation of various cell populations,

depending on their surface antigens. This

method allows cells to be separated, by

allowing their incubation with magnetic

nanoparticles which are layered with

antibodies against a particular surface

antigen which causes the cells which express

this antigen, to join the magnetic

nanoparticles. Afterwards, they are placed in

strong magnetic field. During this process,

the cells attached to the nanoparticles which

stay on the column, while the other cells

flow through. With this method, the cells

can be separated with respect to the

particular antigen. Fluorescence-Activated

Cell Sorting (FACS) is a specific type of

flow cytometry. It provides a way for sorting

a heterogeneous mixture of cells into two or

more containers, one cell at a time, based

upon the specific light scattering and the

fluorescent characteristics of each cell. It

also provides a fast, objective and

quantitative recording of the fluorescent

52



signals from individual cells, as well as the

physical separation of the cells which are of

particular interest. The cell surface markers

are useful for classifying and isolating stem

cells and for monitoring their states of

differentiation, because they can be

visualized directly with the intact cells.[32]

Cryopreservation

The haematopoietic stem cells have been

cryopreserved and successfully utilized for

transplantation. The dental pulp can be

easily cryostored for long periods [33] and

can be used to form a cryobank for adult

tissue regeneration.[34] The dental pulp

stem cells retain their potential after

cryopreservation.[35] In a study which was

performed on the cryopreserved tissue

samples of periodontal ligaments [36], the

cryopreservation of the whole dental pulp

leads to safe recovery. Different

cryopreservation techniques are required for

whole pulp. These features make these cells

for a therapeutic three-dimensional tissue

reconstruction, with the potential of storage

and recovery as per the needs of the patient.

Regeneration of the tooth tissue and

blood vessels

SHED have the potential to differentiate into

functional vascular endothelial cells by a

process that resembles

vasculogenesis.[37,38] These findings raise

the hope that the stem cells of dental pulp

origin may be useful in treating severe

ischaemic conditions of the brain,heart, or

the limbs. Production of a functional

vascular network is specifically one of the

challenges of dental pulp tissue engineering,

considering the fact that all vascularizations

must access root canal through the apical

foramen. Hence, more research is needed for

the induction of vasculogenesis

accompanying efforts for dental pulp tissue

engineering.

Whole tooth regeneration

Tooth-like tissues have been generated by

placing the stem cells on biodegradable

scaffolds. Ikeda et al reported a fully

functioning tooth replacement in an adult

mouse, which was achieved by the

transplantation of a bioengineered tooth

germ into the alveolar bone in the lost tooth

region.[39] Xu et al, seeded a tooth bud

from the rat on scaffolds which were

fabricated from silk fibroin, with 2 pore

sizes that were either used as fabricated or

treated with the Arg-Gly-Asp attachment

site binding peptide.[40] Although dental

tissues are regenerated, the success rate for

the correct arrangement of a natural tooth is

53



only 15-20%. So, further studies are

required to achieve structurally sound teeth.

Bone tissue regeneration

When DPSCs undergo differentiation into

pre-osteoblasts, form an extracellular matrix

that becomes a calcified woven bone

tissue.[41] Other than this, it has been

demonstrated that such tissues undergo

remodelling, when they were transplanted in

immunocompromised rats, and with

entrapped osteocytes that they form a

lamellar bone.[42]

In treating various diseases

Stem cells play a vital role in treating

various life threatening diseases. Other than

forming the blood vessels, bone, the whole

tooth and the dental tissues, dental pulp stem

cells can also be used to treat Parkinson’s

disease, myocardial infarction, Diabetes

mellitus and certain forms of cancer. [43]

Source: National Institute of Health.The

promise of stem cell research [figure on the

internet]. Bethesda: NIH; 2009 [cited 2010

May 03]. Available from: http://

alumnimagazine.uconn.edu/sprg2007/featur

e2.html

Figure 1- Diagram depicting the expected

clinical applications of some stem cell

research.[44]

The relative size of the stem cell population

and determining the potential of primary

tooth pulp to signal epithelial cell

differentiation, as occurs in tooth

development.[45]

METHODS

Identifying stem cells from primary

dental pulp.

Modification of “Miura et al” was used to

harvest primary dental pulp as follows. All

cells were obtained with permission from

the Committee on Human Research of the

University of California San Francisco

(UCSF), San Francisco, Calif. Primary teeth

that were extracted for reasons other than

research, such as for orthodontic reasons or

caries, were obtained from the UCSF

Pediatric Dental Clinic. The tooth surface

was cleaned with 10 percent povodine

iodine, rinsed with phosphate buffered saline

(PBS), and cut around the cementum-enamel

54



junction to reveal the pulp chamber. The

pulp tissue was gently separated from the

crown and root and placed in 10 percent

penicillin/streptomycin/fungizone in 4°C

overnight. After digesting in 4 mg/ml

collagenase/dispase (Roche, Indianapolis,

IN) for 4 hours at 37''C, single-cell

suspensions were obtained by passing the

cell mass through a 70-pm strainer. These

cells were grown on Falcon tissue culture

dishes (Becton/Dickinson, San Jose, CA)

with Dulbecco's modified Eagle's medium

(DMEM) low glucose, supplemented with

10 percent fetal bovine serum (PBS) and 1

percent penicillin/streptomycin.

Immunolocalization of stem cells.

First passage cells were grown on chamber

slides until 80% confluent. The cells were

fixed in precooled 4 % paraformaldehyde

(PFA) for 10 minutes and washed 3 times

with PBS. The cells were then incubated

with 0.1% TritonX-1OO/ PBS for 15

minutes at room temperature before

blocking with 3% bovine serum albumin in

PBS. The cells were incubated overnight at

4°C with:

1. Rabbit antihuman antibodies against

STRO-1 (1:200 dilution, R&D

Systems, Minneapolis, MN), which

is a mesenchymal stem cell marker;

2. CD146 (1:100 dilution, R&D

Systems), another mesenchymal

stem cell marker;

3. Collagen type-I, (1:100 dilution,

Santa Cruz, Calif), the primary

matrix protein synthesized by

odontoblasts and pulp fibroblasts;

and

4. Amelogenin (1:1,000 dilution), the

primary matrix protein synthesized

by ameloblasts.

Amelogenin antibody was generated from

recombinant human amelogenin immunized

rabbits. After thorough washing, the cells

were stained by fluorescence-labeled

secondary antibodies for 1 hour, and nuclei

were counter-stained with 1 µg/ml Hoechst

33342 (Molecular Probes, Carlsbad, CA),

and photographed using a Nikon Eclipse 300

microscope and digital imaging system

(QIMAGING digital camera, QIMAGING,

Surrey, BC, Canada) and SimplePCI

software, (QIMAGING, Surrey, BC,

Canada).

Fluorescence-activated cell sorting

(FACS).

Primary tooth pulp tissue was gently

separated from the crown and root and

55



placed overnight in 10 percent

penicillin/streptomycin/ fungizone at 4°C.

Then The pulp tissue was digested in 4

mg/ml collagenase/dispase (Roche) for 4

hours at 37''C. Single cells were isolated and

incubated with STRO-1 antibody for 1 hour

and then followed by incubation with

fluoresceinisothiocyanate-labeled secondary

antibody for 1 hour. The cells were sorted

using a FACS machine, and the % of STRO-

1 positive cells was determined.

Oral epithelial cell cultures

Buccal mucosa was isolated from 18- to 22-

week human fetal tissue, obtained

underguidelines set by UCSF. The tissue

was digested in 2 mg/ml collagenase/dispase

for 1 hour at 37°C, washed with PBS, and

further digested with STV (0.05 percent

trypsin, 0.025 percent versene) for 5

minutes. The cells were pelleted and washed

with PBS, and lx105cells were plated on a

100 mm Primaria tissue culture dish (Becton

Dickinson Labware, Franklin Lakes, NJ)

and fed with supplemented keratinocyte

media (KGM-2, Cambrex, Walkersville,

Md) with 0.05 mm calcium. This medium is

selective for epithelial cells, and inhibits

growth of fibroblasts. The medium was

changed every other day. Passage 1 (PI)

cells were characterized for cytokeratin l4

(an epithelial cell marker) by

immunocytochemistry.

Coculture of dental pulp cells and oral

epithelial cells.

Dental pulp cells from primary teeth (pDPC)

were growth arrested by gamma radiation.

Briefly, initial passage (PO)pDPCs were

grown to 80 percent confluence in DMEM

low glucose supplemented with 10 percent

FBS and 1 percent penicillin/streptomycin.

The cells were trypsinized with STV, rinsed

with PBS, and gamma irradiated at 5000

rad. The irradiated pDPCs were plated on

Petri dishes (2x105cells) and chamber slides

(1x105cells) with DMEM low glucose

supplemented with 10 percent FBS and 1

percent penicillin/streptomycin. Twenty-

four hours later, first passage oral epithelial

cells (OEC) were plated onto the same Petri

dishes and chamber slides. The coculture

cells were grown in modified DMEM

containing a low calcium concentration of

0.05 mm calcium to enhance epithelial cell

growth and supplemented with 10 percent

FBS and 1 percent penicillin/streptomycin.

The medium was changed every 2 days. As

controls, pDPCs were plated alone and

OECs were plated alone and grown in the

same modified DMEM for the same length

of time. On day 3, the dishes of control cells

56



and cocultured OECs and irradiated pDPCs

were collected and prepared for real-time

polymerase chain reaction (PCR). The

chamber slides were all fixed with precooled

4 percent PFA and washed 3 times with PBS

in preparation for immunostaining. The cells

were immunostained for both cytokeratin 14

and amelogenin.

Total RNA was extracted from the cells

using RNeasy Mini Kit (Qiagen, Valencia,

Calif). The mRNA was transcribed into

cDNA with random primer and Superscript

reverse transcriptase (Invitrogen, Carlsbad,

Calif). Amplification with amelogenin gene-

specific primers (Applied BioSystems,

Foster City, Calif) was done using an

Applied BioSystems real time PCR

machine, model no. 7599, using 18S RNA

as a control.[46]

DEVELOPMENTAL POTENTIAL

Differentiation Potential of DPSCs in

Vitro.

Long-term cultures (5–6 weeks) of DPSCs

grown in the presence of L-ascorbate-2-

phosphate, the glucocorticoid,

dexamethasone, and inorganic phosphate

demonstrated the capacity to form Alizirin

Red positive condensed nodules with high

levels of calcium (Fig. 2A). The deposits

were sparsely scattered throughout the

adherent layer as single mineralized zones.

In contrast, BMSC cultures produced

extensive sheets of calcified deposits over

the entire adherent layer after 3–4 weeks of

induction (Fig. 2C). After 6 weeks of

stimulation with dexamethasone, there was

no evidence of adipogenesisin primary

DPSC cultures (Fig. 2C), whereas clusters of

lipid-containing adipocytes were detected in

primary cultures of BMSC as early as 2

weeks (Fig. 2D).

Ex Vivo Expanded DPSCs Can Generate

a Dentin Pulp-Like Structure in Vivo.

Because complete developmental potential

and formationof an appropriate histological

structure often cannot be fullyrealized in

vitro, DPSCs were transplanted in

conjunction with HAyTCP powder into

immunocompromised mice. After 6weeks

posttransplantation, DPSCs generated a

dentin-like structure lining the surfaces of

the HAyTCP particles, comprised of a

highly ordered collagenous matrix deposited

perpendicular tothe odontoblast-like layer

when viewed by polarized light (Fig. 3 A, C,

and D).

57



Figure 2: Developmental potential in vitro.

Adherent layers of cultured DPSCs (A and

B), and BMSCs (C and D) are shown with

Alizarin Red staining as a measure of

calcium accumulation after 6 weeks of

induction with L-ascorbate- 2-phosphate and

dexamethasone with inorganic phosphate (A

and C). After 6 weeks in the same medium

but without inorganic phosphate, lipid

accumulation was noted in BMSCs (D), but

not in DPSCs (B).[47]

Figure 3: Developmental potential in vivo.

Cross sections are representative of DPSC

transplants (A, C, and D) and BMSC

transplants, (B, E, and F) 6 weeks post

transplantation and stained with hematoxylin

and eosin. In the DPSC transplants, the

HAyTCP carrier surfaces (c) are lined with a

dentin-like matrix (d), surrounding a pulp-

like tissue with blood vessels (bv) and an

interface layer of odontoblast-like cells (od)

(A).Amagnified view of the dentin matrix

(d) highlights the odontoblast-like layer (od)

and odontoblast processes (arrow) (C).

Polarized light demonstrates perpendicular

alignment (dashed lines) of the collagen

fibers to the forming surface (D). In BMSC

transplants, lamellar bone (b) is formed on

the HAyTCP surfaces (c) and surrounds a

vascular, hematopoietic marrow organ (hp)

with accumulated adipocytes (a) (B). A

magnified view shows that the new bone

58



contains osteocytes (oc), embedded within

the calcified matrix, and osteoblasts (ob)

lining the bone surfaces (E). With polarized

light, collagen fibrils are seen to be

deposited parallel with the forming surface

(dashed lines) (F).[47]

ETHICAL ISSUES RELATED TO USE

OF STEM CELLS

Stem cell research has political, social,

ethical, and legal issues, creating challenges

for regulatory bodies, policy makers, and

scientists, as they traverse their way through

a tangled web of regulations and moral

proselytizing. Stem cell research raises a

number of such issues, which seem to fall

naturally into two groups:

1) Issues surrounding the origins of stem

cells, in particular, the use of embryo stem

cells. Even if it is assumed or determined

that the source embryos would never have

been enabled to develop as individuals, use

of such tissues does raise assumptions about

status of embryos, which have to be

addressed.

2) Issues relating to the use of stem cell

tissue. In general, the issues are similar to

those relating to organ donation and focus

on the need for appropriate regulation. In its

entirety, medical science is concerned with

interventions, whether preventive,

therapeutic, surgical, emergency, or aimed at

improving quality of life and recommending

healthy lifestyle choices.[48]

CONCLUSION

Virtually every tissue in the body contains

some type of stem cell. From here the idea

of medical and specifically dental cell based

strategies for tissue repair arises. The focus

of stem cell research as it applies to dentistry

is on facial reconstruction. Recent findings

and scientific research supports the use of

these very powerful mesenchymal stem cells

found within teeth and other accessible

tissue harvested from the oral cavity for use

in regenerative medicine. While we can see

the promise of human stem cell therapies for

the future, dentists should know how

important it is to harvest and store these

mesenchymal stem cells, making these

opportunities available to their child,

adolescent, and adult patients for future

regenerative therapies.

REFERENCES

1. Reznick JB. Stem Cells: Emerging

medical and dental therapies for the

dental professional. Dent Town Mag

2008;9:42-50.

2. Becker AJ, McCulloch EA, Till JE.

Cytological demonstration of the

59



clonal nature of spleen colonies

derived from transplanted mouse

marrow cells. Nature 1963;197:452-

4.

3. Govindasamy V, Ronald VS,

Abdullah AN et al. Differentiation

of dental pulp stem cells into islet-

like aggregates. J Dent Res

2011;90:626-52.

4. Kadar K, Kiraly M, Porcsalmy B et

al. Differentiation potential of stem

cells from human

dental origin – Promise for tissue

engineering. J Physiol Pharmacol

2009;60:167-75.

5. Nourbakhsh N, Soleimani M,

Taghipour Z, et al. Induced in vitro

differentiation of neural-like cells

from human exfoliated deciduous

teeth-derived stem cells. Int J Dev

Biol 2011;55:189-95.

6. Nishino Y, Yamada Y, Ebisawa K,

et al. Stem cells from human

exfoliated deciduous teeth (SHED)

enhance wound healing and the

possibility of novel cell therapy.

Cytotherapy 2011;13:598-605.

7. Sloan AJ, Waddington RJ. Dental

pulp stem cells: what, where, how?

International Journal Of Paediatric

Dentistry 2009;19:61–70.

8. Jamal M, Chogle S, Goodis H et al.

Dental Stem Cells and Their

Potential Role in Regenerative

Medicine. J Med Sci 2011;4:53-61.

9. Srisawasdi S, Pavasant P. Different

roles of dexamethasone on

transforming growth factor-beta1-

induced fibronectin and nerve

growth factor expression in dental

pulp cells. Journal of

Endodontics.2007;33;1057–60.

10. Iohara K, Zheng L, Ito M et al. Side

population cells isolated from

porcine dental pulp tissue with self-

renewal and multipotency for

dentinogenesis, chondrogenesis,

adipogenesis, and neurogenesis.

Stem Cells. 2006;24:2493–503.

11. Jo YY, Lee HJ, Kook SY. Isolation

and characterization of postnatal

Stem cells from human dental

tissues.Tissue Engineering.

2007;13:67–73.

12. Chamberlain G, Fox J, Ashton B et

al. Concise review: mesenchymal

stem cells: their phenotype,

differentiation capacity,

immunological features, and

60



potential for homing. Stem Cells.

2007;25:2739-49.

13. JJiang Y, Jahagirdar BN, Reinhardt

RL et al. Pluripotency of

mesenchymal stem cells derived

from adult marrow. Nature.

2002;4;418-9.

14. Gronthos S, Mankani M, Brahim J

et al. Postnatal human dental pulp

stem cells (DPSCs) in vitro and in

vivo. Proc Natl Acad Sci.

USA.2000;97:13625–30.

15. Miura M, Gronthos S, Zhao M et al.

stem cells from human exfoliated

deciduous teeth. Proc Natl Acad Sci.

USA.2003;100:5807–12.

16. Sonoyama W, Liu Y, Fang D et al.

Mesenchymal stem cell mediated

tooth regeneration in swine. PLoS

One. 2006;1:79.

17. Young CS, Terada S, Vacanti JP et

al. Tissue engineering of complex

tooth structures on biodegradable

polymer scaffolds. J Dent Res.

2002;81:695–700.

18. Ohazama A, Modino SA, Miletich I

et al. Stem-cell-based tissue

engineering of murine teeth. J Dent

Res. 2004;83:518–22.

19. Cordeiro MM, Dong Z, Kaneko T et

al. Dental pulp tissue engineering

with stem cells from exfoliated

deciduous teeth. J

Endod.2008;34:962–69.

20. Sakai VT, Zhang Z, Dong Z et al.

Stem cell differentiate into

functional odontoblasts and

endothelium. J Dent Res.

2010;89:791-6.

21. Demarco FF, Casagrande L, Zhang

Z et al. Effects of morphogen and

scaffold porogen on the

differentiation of dental pulp stem

cells. J Endo.36:1805–11.

22. Casagrande L, Demarco FF, Zhang

Z et al. Dentin-derived BMP-2 and

odontoblast differentiation.J Dent

Res. 2010;89:603–8.

23. Masthan K M, AravindhaBabu N,

Leena S et al. Teeth – as a life bank

(stem cells in dentistry), review

article. Journal of Medicine and

Medical Sciences.2012;3:456-8.

24. Smith AJ, Lesot H. Induction and

regulation of crown dentinogenesis:

embryonic events as a template for

dental tissue repair? Crit Rev Oral

Biol Med. 2001;12:425–37.

61



25. Smith AJ, Murray PE, Sloan AJ et

al. Transdentinal stimulation of

tertiary dentinogenesis. Adv Dent

Res. 2001;15:51–4.

26. Tziafas D. Basic mechanisms of

cytodifferentiation and

dentinogenesis during dental pulp

repair. Int J DevBiol. 1995;39:281–

90.

27. Graham L, Cooper PR, Cassidy N et

al. The effect of calcium hydroxide

on solubilisation of bio-active

dentine matrix components.

Biomaterials. 2006; 27:2865–73.

28. .Fitzgerald M, Chiego DJ, Heys DR.

Autoradiographic analysis of

odontoblast replacement following

pulp exposure in primate teeth. Arch

Oral Biol. 1990;35:707–15.

29. Smith AJ, Cassidy N, Perry H,

Begue-Kirn C, Ruch JV, Lesot H.

Reactionary dentinogenesis. Int J

Dev Biol. 1995;39:273–80.

30. Murray PE, Smith AJ. Saving pulps:

a biological basis.An overview.Prim

Dent Care. 2002;9:21–6

31. .Thomas BB, Leoni A, Kunz S et al.

Cancer Stem Cells as a Predictive

Factor in Radiotherapy. Seminars in

Radiation Oncology, 2012;22:151–

74.

32. Kohji N, Yoko Y, Toshiaki I. Cell

surface biomarkers of embryonic

stem cells, Proteomics.

2008;8:4025–35.

33. Papaccio G, Graziano A, Aquino R

et al. Long-term cryopreservation of

dental pulp stem cells (SBP-DPSCs)

and their differentiated osteoblasts:

A cell source for tissue repair.

Journal of Cellular Physiology.

2006;208:319–25.

34. Graziano A, Biunno I, Blasio DP et

al. The tissue banking in cancer and

stem cell research. Journal of

Cellular Physiology. 2007;212:345–

7.

35. Zhang W, Walboomers XF, Shi S et

al. Multilineage differentiation

potential of stem cells derived from

human dental pulp after

cryopreservation. Tissue

Engineering. 2006;12:2813–23.

36. Seo BM, Miura M, Sonoyama W et

al. Recovery of stem cells From

cryopreserved periodontal ligament.

Journal of Dental Research.

2005;84:907–12.

62



37. Cordeiro MM, Dong Z, Kaneko T et

al. Dental pulp tissue engineering

with stem cells from exfoliated

deciduous teeth. J Endod.

2008;34:962–9.

38. Sakai VT, Zhang Z, Dong Z et al.

SHED differentiate into functional

odontoblasts and endothelium. J

Dent Res. 2010;89:791–6.

39. Ikeda E, Morita R, Nakao K et al.

Fully functional bioengineered tooth

replacement as an organ

replacement therapy. Proc Natl

AcadSci USA. 2009;106:13475–80.

40. Xu WP, Zhang W, Asrican R et al.

Accurately shaped toothbud cell-

derived mineralized tissue

formation on silk scaffolds. Tissue

Eng Part A. 2008;14:549–57.

41. Laino G, Aquino R, Graziano A et

al. Dental pulp stem cells can be

detected in aged humans: an useful

source for living autologous fibrous

bone tissue (LAB). J Bone Miner

Res. 2005;20:1394–402.

42. Laino G, Graziano A, Aquino R et

al. An approachable human adult

stem cell source for hard-tissue

engineering. J Cell Physiol.

2006;206:693–701.

43. Yapeng Hu, Liwu Fu Targeting

cancer stem cells: a new therapy to

cure cancer Patients. Am J Cancer

Res. 2012;2:340-56.

44. Telles PD, Machado MAAM, Sakai

VT et al. Pulp tissue from primary

teeth: new source of stem cells. J

Appl Oral Sci.2011;19:189-94.

45. Coppe C, Zhang Y, Besten PKD.

Characterization of Primary Dental

Pulp Cells In Vitro.PediatrDent.

2009;31:467.

46. Baume LJ. Dental pulp conditions in

relation to carious lesions. Int Dent J

1970;20:309-37.

47. Gronthos E.Postnatal human dental

pulp stem cells (DPSCs) in vitro and

in vivo.PNAS.2000;97:13625–30.

48. Longstaff H, Schuppli CA, Preto N

et al. Scientists perspectives on the

ethical issues of stem cell research.

Stem Cell Rev 2009;5:89-95.

63

REVIEW ARTICLE


The Self Adjusting Files: A Step Closer Towards Perfection

Dr. Pravek Khetani 1, Prof (Dr.) Usha Dabas

2, Prof (Dr.) Vipin K. Dabas

3

1Post Graduate Student, Dept. Of Conservative Dentistry and Endodontics,

2 Professor & HOD, Dept. of

Conservative Dentistry and Endodontics, 3 Professor, Dept. of Conservative Dentistry and Endodontics,

Vyas Dental College & Hospital, Pali road, Jodhpur. Rajasthan, India.

INTRODUCTION:

Rotary nickel titanium (NiTi) files were first

introduced clinically in 1993. They were a

major turning point and represented a real

paradigm shift in endodontics.[1,2] New

designs have been introduced over the years,

attempting to make these instruments more

efficient, more flexible, and safer in terms of

file separation.[3]

The targets of endodontic treatment are the

complete cleaning, adequate disinfection, and

effective obturation of the root canal.[4] Each

of these challenging targets is critical for the

success of endodontic treatment and operators

are expected to do as complete a job as

possible in each of these targets to ensure

endodontic success.[5]

Current rotary file systems are effective tools

but they have few shortcomings, like, they are

unable to effectively clean and shape oval

canals and depend too much on the irrigant to

do the cleaning of the canals and also they

unnecessarily remove excessive sound dentin

and create micro cracks in the remaining root

dentin which in turn might question the

prognosis of the tooth.[6,7]

The current

ABSTRACT:

The Self-adjusting File (SAF) technology uses a hollow, compressible NiTi file,

through which a continuous flow of irrigants is provided throughout the procedure.

The SAF technology provides effective cleaning of all root canals including oval

canals, thus allowing for the effective disinfection and obturation of all canal

morphologies. This technology uses a new concept of cleaning and shaping in which

a uniform layer of dentin is removed from around the entire perimeter of the root

canal, thus avoiding unnecessary excessive removal of sound dentin. The mode of

action used by this file system does not apply the machining of all root canals to a

circular bore, as do all other rotary file systems, and does not cause micro-cracks in

the remaining root dentin. The new SAF technology allows for a minimally invasive

cleaning and shaping root canals.

KEY WORDS: SAF, NiTi file, cleaning and shaping, rotary file, minimally

invasive.

64

The Self Adjusting Files: A Step Closer Towards Perfection Khetani P et al


instruments were designed ignoring the

natural 3D shape of many of the root canals,

and therefore, they clean and shape all canals

as if they were narrow, straight canals with

round cross-sections.[8,9] By using these

instruments, operators are often actually

treating an imaginary tooth rather than

addressing the 3D reality of a given root

canal.[10]

The aim of this review is to introduce the

reader to the SAF System and its mode of

operation. The new concept of minimally

invasive 3D endodontics has emerged, made

possible by the new SAF technology.[5] This

concept aims to achieve all of the basic aims

of root canal treatment without causing the

unnecessary damage to the radicular dentin

often observed in roots treated with

traditional, old, or new rotary file

instrumentation.[5,11,12,13,14,15]

DESIGN AND MODE OF OPERATION

The SAF is a hollow

file designed as a

compressible, thin-

walled pointed

cylinder either 1.5 or

2.0 mm in diameter

composed of 120-μm-

thick nickel-titanium

lattice.[16] The SAF

system is extremely flexible and also extremely

compressible, so that a 1.5-mm diameter SAF

may be compressed into a root canal in which

only a #20 K file could previously be

inserted.[8,16] The file will then attempt to

regain its original dimensions, thus applying a

constant delicate pressure on the canal walls.[8]

When inserted into a root canal, it adapts itself

to the canal's shape, both longitudinally and

along the cross-section.

In a round canal, it will attain a round cross-

section, whereas in an oval or flat canal it will

attain a flat or oval cross-section, providing a

three-dimensional adaptation.[8] The surface of

the lattice threads is lightly abrasive, which

allows it to remove dentin with a back-and-

forth grinding motion.[16] The SAF consist of

a Shank(friction grip), Rubber stopper,

irrigation barb, and a shaft.

The RDT handpiece

Fig 1: The SAF

Fig 3: The various parts of SAF

Fig 2: The NiTi Lattice of SAF

65



The RDT handpiece-head has a dual

mechanical

function. It turns

the rotation of the

micro-motor into a

trans-line in-and-

out vibration with

an amplitude of

0.4 mm.[8]It also

contains a clutch mechanism that allows the

SAF to rotate slowly when not engaged in the

canal but completely stops the rotation once

the file is engaged with the canal walls.[9]

The micromotor is operated at 5000 rpm,

which results in 5000 vibrations/min, and the

operator uses pecking motions when using the

SAF.[8] Free rotation of the file should occur

at every out-bound part of every pecking

stroke, when the SAF file is disengaged from

the canal walls.[17]

This is required to ensure that when the SAF

enters the canal during the in-bound pecking

motion, it will do so at a different, random

circular position every time, thus ensuring

uniform treatment of the canal walls.[8,17,18]

The Irrigation Pump

The irrigation pump is a self-contained

peristaltic pump with a built-in irrigant

reservoir of 500ml operated using a foot

switch and powered by a rechargeable

battery.[8]The SAF file is provided with a

freely rotating hub connected to a

polyethylene tube thus allowing for flow of

the irrigant through the hollow file and into

the root canal.(9) The irrigant can be

delivered into the tube at a rate ranging from

1-10 ml per minute, with the typical

recommended setting of 4 ml per minute. (9)

The SAF is inserted into the canal while

vibrating and is delicately pushed in until it

reaches the predetermined working length. [8]

It is then operated with in-and-out manual

motion and with continuous irrigation using

two cycles of 2 minutes each for a total of 4

minutes per canal. This procedure will

remove a uniform dentin layer 60 to 75-μm

thick from the canal circumference. [8]

Continuous Irrigation with Sodium

Hypochlorite

Irrigation of the root canal with copious

amounts of sodium hypochlorite during root

Fig 4: The RDT handpiece

Fig 5: The mode of action of

the SAF

Fig 6: The irrigation pump for the SAF

66



canal treatment is widely

recommended.[19,20] It has been well

documented that when exposed to its target of

bacteria and tissue debris, sodium

hypochlorite loses its activity rather

quickly.[21] Taking into account the

extremely small volume of the root canal, the

amount of sodium hypochlorite contained in

the canal loses its activity within a very short

time.[19] Therefore, as frequent replacement

of the irrigant as possible is mandatory for

maintaining its optimal potency and

effect.[19]

The SAF operates with a continuous flow of

the irrigant, thus allowing continuous fresh

irrigant to be present in the canal at all

times.[22] The vibration of the file's metal

lattice within the irrigant facilitates its

cleaning and debridement effects.[22,23]

Effective sodium hypochlorite replacement in

the apical part of the canal is essential to

provide its full effect and benefits in this

critical area during root canal treatment.[24]

Drawbacks of SAF

The SAF is also subject to the risks of

mechanical failure. When mechanical failure

of the SAF occurs, it is most often in the form

of tears in the lattice.[8,16,25,26] Such

failures might be limited to either: (a) Partial

detachment of an arch or strut at one end; or

(b) full detachment of an arch.[26]

Fig7A: An intact SAF file. B: Arch detachment in

an SAF file. C: Several arch detachments in an SAF

file.

These two types of mechanical failure are

usually of no clinical consequence, other than

having to replace the file. In cases of the

partial detachment of an arch, the file should

simply be discarded. In cases of full

detachment of an arch, the detached arch is

easily washed out, using either the action of

SAF irrigation and movement or ultrasonic-

assisted irrigation.[26]

CONCLUSION:

The SAF represents a new approach in

endodontic file design and operation. Its main

features are as follows:

A three-dimensional adaptation to the

shape of the root canal, including

adaptation to its cross-section.[8]

One file is used throughout the

procedure, during which it changes from

an initially compressed form to larger

dimensions.[8]

B

C

67



Canal straightening and canal

transportation of curved canals are

largely avoided because of the lack of a

rigid metal core. The file does not have

“a will of its own.”[8]

High mechanical durability, thus

overcoming the issue of separated

nickel-titanium instruments.

Hollow design that allows continuous

irrigation with constant refreshment of

the irrigant throughout the procedure.

REFERENCES:

1) De Chevigny C, Dao TT, Basrani BR, Marquis

V, Farzaneh M, Abitbol S, et al. Treatment

outcome in endodontics: The Toronto study-phase

4 : i0 nitial treatment. J Endod 2008;34:258-63.

2) Molander A, Caplan D, Bergenholtz G, Reit C.

Improved quality of root fillings provided by

general dental practitioners educated in nickel-

titanium rotary instrumentation. Int Endod J

2007;40:254-60.

3) Larsen CM, Watanabe I, Glickman GN, He J.

Cyclic fatigue analysis of a new generation of

nickel titanium rotary instruments. J Endod

2009;35:401-3.

4) Peters OA, Peters CI, Schönenberger K,

Barbakow F. ProTaper rotary root canal

preparation: Effects of canal anatomy on final

shape analysed by micro CT. Int Endod

J. 2003;36:86–92.

5)Shemesh H, Bier CA, Wu MK, Tanomaru-Filho

M, Wesselink PR. The effects of canal

preparation and filling on the incidence of

dentinal defects. Int Endod J 2009;42:208-13.

6)Wu M-K, Wesselink PR. A primary observation

on the preparation and obturation in

oval canals. Int Endod J 2001;34:137–41.

7)Wu M-K, van der Sluis LWM, Wesselink PR.

The capacity of two hand instrumentation

techniques to remove the inner layer of dentin in

oval canals. Int Endod J 2003;

36:218–24.

8) Metzger Z, Teperovich E, Zary R, Cohen R,

Hof R. The self-adjusting file (SAF). Part 1 :

Respecting the root canal anatomy-a new concept

of endodontic files and its implementation. J

Endod 2010;36:679-90.

9)Metzger Z. From Files to SAF : 3D endodontic

treatment is possible at last. Alpha Omega

2011;104:3644.

10)Metzger Z, Kfir A, Abramovitz I, Weissman

A, Solomonov M. The Self-adjusting File

system. ENDO (Lond Eng) 2013;7:189-210.

11) Bier CA, Shemesh H, Tanomaru-Filho M,

Wesselink PR, Wu MK. The ability of different

nickel-titanium rotary instruments to induce

dentinal damage during canal preparation. J

Endod 2009;35:236-8

12) Adorno CG, Yoshioka T, Suda H. Crack

Initiation on the apical root surface caused by

three different nickel-titanium rotary files at

different working lengths. J Endod 2011;37:522-

5.

13) Yoldas O, Yilmaz S, Atakan G, Kuden C,

Kasan Z. Dentinal microcrack formation during

root canal preparations by different Ni-Ti rotary

instruments and the self-adjusting file. J Endod

2012;38:232-5.

14) Hin ES, Wu MK, Wesselink PR, Shemesh H.

Effects of self-adjusting file, Mtwo, and ProTaper

on the root canal wall. J Endod 2013;39:262-4.

15) Liu R, Kaiwar A, Shemesh H, Wesselink PR,

68



Hou B, Wu MK. Incidence of apical root cracks

and apical dentinal detachments after canal

preparation with hand and rotary files at different

instrumentation lengths. J Endod 2013;39:129-

32.

16)Hof R, Perevalov V, Eltanani M, Zary R,

Metzger Z. The self-adjusting-file (SAF). Part

2 : Mechanical analysis. J Endod

2010;36:691-6.

17)Metzger Z, Kfir A, Abramovitz I,

Weissman A, Solomonov M. The Self-

adjusting File system. ENDO (Lond Eng)

2013;7:189-210.

18) Peters OA, Paqué F. Root canal

preparation of maxillary molars with the Self-

Adjusting File A micro-computed

tomography study. J Endod 2011;37:53-7.

19) Estrela C, Estrela CRA, Barbin EL, et al.

Mechanism of action of sodium hypochlorite.

Braz Dent J 2002;13:113–7.

20) Buchanan LS. The standardized-taper root

canal preparation: part 3. GT file technique in

large root canals with small apical diameter.

Int Endod J 2001;34:149–56.

21) Haapasalo M, Qian W. Irrigants and

intracanal medicaments. In: Ingle JI, Bakland

LK, Baumgartner JC, eds. Ingle’s

Endodontics. 6th ed. Hamilton, Canada: BC

Deker Inc; 2008:992–1018

22) Sena NT, Gomes BPFA, Vianna ME, et

al. In vitro antimicrobial activity of sodium

hypochlorite and chlorhexidine against

selected single-species biofilms. Int Endod J

2006;39:878–85.

23) Metzger Z, Teperovich E, Cohen R, et al.

The Self Adjusting File (SAF). Part 3:

Removal of debris and smear layer. A

scanning electron microscope study. J Endod

(in press)

24) Peters OA, Peters CI. Cleaning and

shaping of the root canal system. In: Cohen S,

Hargreaves KM, eds. Pathways of the Pulp.

9th ed. St Louis, MO: Mosby; 2006: 290–357.

25) Metzger Z. The self-adjusting file (SAF)

system: An evidence-based update. J Conserv

Dent.2014;17:401–19

26) Farmakis ET, Sotiropoulos GG, Pantazis

N, Kozyrakis K. The permanent deformation

of the self-adjusting files when used in canals

of extracted teeth. Int Endod J. 2013;46:863–

9

69

REVIEW ARTICLE


CESSATION: AN ESSENTIAL COMPONENT FOR GLOBAL PUBLIC HEALTH - A

REVIEW Dr. Sweta Soni

1

1Reader, Vyas dental college and hospital, Jodhpur

Department of Periodontics, Vyas Dental College and Hospital, Pali road, Jodhpur, Rajasthan

Introduction

1.2 billion tobacco users has been estimated

worldwide, which is expected to rise to 1.6

billion during 2025.[1,2] At present,

tobacco use causes death of 3.5 to 4 million

people globally, which is expected to

increase to about 10 million during

2025.[1,2,3] Tobacco is used for smoking as

well as in smokeless form. Smoking of

tobacco is mainly in the form of bidi,

cigarette, hukah, chilum, chutta, etc. The

habit of smokeless tobacco (also referred as

tobacco chewing) is also very common.

Some common forms of smokeless tobacco

ABSTRACT:

Tobacco cause a dentrimental effect on the health and well-being of the public and

75 percent of deaths resulting from oral and pharyngeal cancer. All over the world,

studies show that people who quit tobacco live longer than people who continue to

use tobacco. This however is dependent on various factors such as the tobacco use

pattern, duration and existence of illness at the time of quitting. Considering the

extensive use and benefits of cessation, starting tobacco cessation clinics in different

health settings and training health providers in cessation seemed to be the need of

the hour, apart from various community awareness and socio-legal initiatives

primarily aimed at prevention. Cessation of tobacco use is the most significant

actions a personcan take to secure their health − both oral and general. Any health

care professional can provide tobacco cessation services. However pharmacological

interventions can be carried out only by medical practitioners. Health care

practitioners include Doctors, Psychologists, Social Workers, Nurses and Dental

professionals. The potential role of the dental team in assisting this process is now

well recognized. This review article presents the impact of tobacco use on health

and outlines current evidence on the role of the dental team in helping patients in

tobacco cessation and control measures.

KEY WORDS: Five As Program, Nicotine Addiction, Pharmacotherapy Smoking

Tobacco, Smokeless Tobacco, Tobacco Cessation, Tobacco Cessation Policy.

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70

CESSATION: AN ESSENTIAL COMPONENT FOR GLOBAL PUBLIC HEALTH Soni S et al


include khaini, Mainpuri tobacco, mawa,

mishri, etc.[4,5,6,7] Tobacco use cause

various diseases for example 30% of all

cancers, 90% of all lung disease, 30% of all

ischaemic heart disease and strokes, and

70% of all chronic lung disease (Peto et al.,

1996).[8] The most common effects of

smoking on the oral cavity are like oral

cancers and pre-cancers; increased severity

and extent of periodontal diseases; and poor

wound healing. (Allard et al., 1999).[9]

Recent studies has suggested that chewing

tobacco causes both oral and pancreatic

cancers (Cogliano et al., 2004).[10]

So, the prevention and control of tobacco

use is a significant issue of oral as well as

systemic health It. could become one of the

most important oral health issues of the

twenty-first century.[11,12] Significant

number of smokers wants to quit, but only

30% try each year and only 3-5% actually

achieve this. In people who have managed to

quit tobacco use, the body starts repairing

itself within 24 hours of quitting.[13,14] In

one year, heart disease death rate is half that

of a smoker. In 5 years, stroke risk drops

nearly to that of non-smokers. In 10 years,

lung cancer risk drops to 50%.iv. Nicotine

from tobacco, whether smoked or chewed, is

highly addictive, and therefore stopping is a

major challenge for most users.[15,16] Over

a 12-month period, nearly half of smokers

will make a quit attempt, but only a very

small number will successfully stop

unassisted. Cessation rates are lowest

amongst more dependent smokers.[17]

Dental teams are ideally placed to get

actively involved in tobacco cessation

activity. Surveys indicate that dental teams

have an increasingly positive attitude

towards tobacco cessation and are becoming

more actively involved (John et al., 2003;

Johnson et al., 2006).[18,19]

History of development of tobacco

cessation policies :

The first Surgeon General’s report, Smoking

and Health, was released in 1964. The

nature and power of nicotine addiction were

not widely understood until the 1988 release

of the Surgeon General’s report on Nicotine

Addiction.[2] Quitting methods varied

widely from the 1960s through the 1980s

and were primarily empirical. In 1970,

Christen was among the first to suggest

specific guidelines for dental office-based

smoking cessation activities.[20,21] In

1980s, Indiana University, the University of

Kentucky, and the National Cancer Institute

encourage oral health team members to

become active in tobacco education, control

and cessation.[22]

Tobacco interventions

shifted away from cessation services

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71



towards social policy strategies, such as the

promotion of clean air laws, measures that

would reduce initiation by children and

youths, litigation for health and economic

harm, law enforcement, and the exposure of

tobacco industry tactics.

During the 1990s, four major events

occurred for treating tobacco use and

dependence:

New technology permitted

examination of central nervous

system and abnormal brain function.

Brain scans, microsensors,

radioisotopes yielded fresh insight

about the influence of psychotropic

drugs, and particularly nicotine, on

perception, and behavior.

At the clinical level, findings from

various intervention studies led to

the 1996 clinical practice guideline,

Smoking Cessation,[23] and the

2000 guideline, Treating Tobacco

Use and Dependence.[24]

A variety of pharmacotherapies were

found to effectively augment

behavioral interventions during the

quitting process.[25,26]

Studies now range from the micro-

level (e.g., molecular and cellular),

across the individual level (e.g.,

genetic, perceptual, experiential), to

the macro-level (e.g., societal,

cultural, environmental).[27]

Nicotine Addiction:

Nicotine, one of the most addictive chemical

known to mankind, acts on the human brain

and gives a reward comparable to what one

gets when his basic needs are satisfied.

Nicotine is a mood-altering drug if taken

excessively and compulsively, causing

physiologic tolerance, tissue dependence,

psychic dependence, and relatively well

defined physical withdrawal symptoms. The

addictive smoking chain comprised two

links, psychological dependence and socio-

cultural factors, interconnect with the

common core, nicotine addiction.[28] As

nicotine dependence develops, a

corresponding set of emotions and behaviors

perpetuates the act of smoking. Most

commonly noticed withdrawal symptoms in

the case of nicotine withdrawal are

irritability, decreased concentration and

decreased interest to socialize, restlessness

and headache. Once the person satisfies his

brain's urge to have the next fix of nicotine,

withdrawal symptoms subside temporarily.

This cycle continues and this is when one is

said to be having biological dependence.[29]

STRATERTGIES FOR TOBACCO

CESSATION:

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72



Individually delivered smoking cessation

counselling can assist smokers to quite.[30]

There are various used in the tobacco

cessation intervention. They are:[31,32]

I) Behavioral Intervention

II) Clinic-based tobacco intervention

measures

- The Five As of tobacco

cessation

- Pharmacotherapy - Nicotine

Replacement Therapy, Other

III) Intervention policies

Behavioral Intervention:

Behavioral interventions are the primary

level of intervention provided to a

quitter. The components of the

behavioral intervention are:[31,33]

- Habit analysis: This involves

maintaining a tobacco diary where

person can record his tobacco

consumption in terms of the time,

place, mood status and the need for

tobacco at that particular time.

Comparison of a few days' diary

facilitates the identification of one's

own distinctive triggers.

- Craving management: Craving or

urge hits the tobacco users more

frequently during the initial weeks of

quitting. It is one of the most

common reasons for lapse in quitters.

Techniques such as the 4 D’s

(Delaying, Distracting, Deep

breathing and Drinking water) can be

easily mastered with proper

guidance.

- Withdrawal management:

Withdrawal symptoms vary from

user to user and hence it is essential

to identify users specific withdrawal

symptoms before advice on ways of

handling them. Quitters experience

physical as well as psychological

withdrawal symptoms and to counter

these, a wide array of techniques

ranging from stress management to

diet modifications can be used.

- Relapse prevention: It is a part of

the cessation process which many of

the users undergo. Many of the

quitters relapse for a few times

before quitting forever. It is very

important for the therapist to

understand that relapse does not

indicate a failure of the intervention

or lack of motivation of the user.

Clinic-based tobacco intervention

measures:[34]

- The Five As of tobacco cessation:

The Five As framework as a guide to

approaching tobacco cessation in a

clinical setting is well known. This

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73



scheme provides an ordered structure

to help healthcare professionals.

Ascertain a patient’s smoking status-

ASK; Provide advice on the benefits

of quitting- ADVISE; Ascertain a

patient’s readiness to quit- ASSESS;

Provide assistance in a quit attempt-

ASSIST; Follow-up the outcome of

quitting- ARRANGE. The steps in

this process are outlined in Table-1.

- Pharmacotherapy: There are many

pharmacological agents which

support in the process of quitting.

These medicines act on the brain to

reduce craving and the withdrawal

symptoms associated with quitting

tobacco.[35,36]

Nicotine Replacement Therapy:

Oral Health Research Institute at

IUSD established the concept that

dentally oriented smoking cessation

programs, utilizing FDA approved

forms of nicotine replacement

therapy (NRT), are both safe and

effective. These investigations

revealed smoking cessation quit rates

ranging from 12 to 26 percent in

those persons using NRT, as

compared to 5-12 percent in

individuals using a placebo product.

Thus, these results clearly

demonstrate that dental team efforts,

accompanied by a structured

behavioral program that utilizes

NRT, produce significant success

rates.[37,38] NRT is a safe means of

helping smokers deal with

withdrawal symptoms. Nicopass,

Nicopatch, Nicorette, Nicotinelle,

Niquitin are different NRT products

currently available in market in the

six different forms (gum, patch,

nasal spray, inhaler, lozenge and

sublingual tablet), all with similar

success rates.[39]

Others: Aside from NRT, the other

effective pharmacotherapy used in

tobacco cessation is

bupropion(Zyban), an atypical

antidepressant. This product is only

available on GP prescription or

through the NHS Stop Smoking

Services. Due to its potential serious

side effects and interaction with

other medications, dentists cannot

prescribe this drug, and this situation

is highly unlikely to change. Another

promising new pharmacotherapy,

varenicline (Champix), became

available as a prescription-only

medicine in the UK in December

2006. There are no serious side

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74



effects or drug interactions

associated with varenicline. Another

medicine used for tobacco cessation

is Nortryptiline. Pharmacological

interventions when used with

behavioral strategies can produce

quit rates of about 25 –30 %.

Pharmacotherapy reliably increase

long-term smoking abstinence

rate.[39,40]

Intervention Policies:

Policy–level interventions would include

levy of taxes ( to raise prices of tobacco

products and as a disincentive for purchase,

especially to youth on the threshold of

tobacco experimentation), regulation of

tobacco products ( for constituents,

emission, health warning and misleading

health claims) and measures to reduced

supply ( ban on sale to youth, curbs on

smuggling and programs to aid tobacco

farmers and workers to switch over to

alternative livelihoods).[41,42]

Interventions at the community level would

involve programs for encourage people with

the knowledge, motivation and skills

required to abandon the use of tobacco habit.

These would also require the creation of

suitable environments to stimulate, support

and sustain healthy lifestyle choices (such as

tobacco-free norms at schools, worksites,

homes, etc.).[43,44]

Tobacco product regulation, testing and

laboratory strengthening: The regulation

of tobacco products aims progressively

reduce the harmful chemicals and alter their

physical characteristics. A Scientific

Advisory Committee on Tobacco Product

Regulation ( SACtob), developed by the

WHO in 2002, provided technical guidance

on matters related to tobacco product

regulation-limitations of testing methods,

setting up of upper limits for toxic

ingredients and their emission.[45]

Challenges in tobacco cessation program:

It has been found out that retaining people in

follow-up leads to better long term

abstinence rates. One of the most

challenging aspects of a clinic based tobacco

cessation service is maintaining regular

follow up of the users. A combination of

behavioral interventions and

pharmacotherapy was found to positively

influence treatment adherence. There are

other factors associated with drop out during

tobacco cessation treatment such as: poor

motivation, severity of nicotine dependence,

presence of psychiatric co-morbidities,

unavailability of medicine or cost of

treatment, failure to stop or reduce tobacco

use, weight gain. A good relationship

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75



between the client and the therapist is seen

to be a predictor for long term follow

up.[46]

Conclusion:

Tobacco Use is the single largest cause of

disease and premature death in the world.

Being the only consumer product which kills

one half of its regular users, tobacco is

directly responsible for 5.4 million deaths

annually. All over the world, studies show

that people who quit tobacco live longer

than people who continue to use tobacco.

Good communication between team

members is essential, as is the delegation of

different roles and responsibilities. Dentists,

for example, may be responsible for

coordinating the team’s activities, assessing

the smoking status of patients, and referring

motivated smokers for specialist support.

Suitably trained dental care professionals

may be more involved in providing

information and support for smokers

attending the dental surgery.

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76



Table - 1. The smoking cessation Five As program.[34]

STEP ACTION

Ask: systematically identify

all tobacco users at every visit

Smokers – Document this in patient’s notes

Ex-smokers – Congratulate and record in patient’s notes

Never smokers – Congratulate and stress benefits to oral health

Advise: strongly urge all

tobacco

users to quit

Advice should be:

Clear: provide an clear message to quit

Strong: give stress on quitting

Personalized: correlated tobacco use to current oral or

other health problems; social, familial and economic costs;

and motivation level or readiness to quit

Assess: determine willingness

to make a quit attempt

For express a positive interest in stopping:

Stress value of receiving professional help and explain

increased chances of success via a formal stop-smoking

service including pharmacological help in overcoming

nicotine addiction.

For those who express a potential interest in stopping:

Emphasize the benefits of quitting on oral and general

health grounds and provide further written material and

information on NHS Stop-Smoking Services.

For those not interested in stopping:

Accept answer in a non-judgemental fashion and make a

note to return to the subject on a future occasion.

Assist: aid the patient in

quitting

Set a quit date, ideally within two weeks.

family, friends and co-workers and ask for understanding

and support.

Anticipate challenges such as nicotine withdrawal

symptoms, particularly during the critical first weeks

Remove tobacco products from environment.

Before they quit, have patients avoid smoking where they

spend a lot of time—work, home or car.

Arrange: schedule follow-up

Contact

At next recall appointment establish outcome of previous

discussion of topic and establish outcome of quit attempt.

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77



References

1. Burns DM, Lee L, Shen LZ, et al.

Cigarette smoking behavior in the

United States. In: Smoking and

tobacco control monograph 8:

changes in cigarette-related disease

risks and their implication for

prevention and control. NIH Publ

No. 97-4213. Bethesda, MD:

National Institutes of Health,

National Cancer Institute, 1997:13-

42.

2. U.S. Department of Health and

Human Services. The health

consequences of smoking: nicotine

addiction—a report of the Surgeon

General. Rockville, MD: U.S.

Department of Health and Human

Services, Public Health Service,

Centers for Disease Control, Center

for Health Promotion and Education,

Office on Smoking and Health,

1988:30.

3. World Health Organization. Tobacco

alert special issue: the tobacco

epidemic—a global public health

emergency. Geneva, Switzerland:

World Health Organization, 1996.

4. Novotny TE, Pierce JP, Fiore MC,

Davis RM. Smokeless tobacco use in

the United States: the Adult Use of

Tobacco Surveys. Natl Cancer Inst

Monogr. 1989;8:25-8.

5. Cigarette smoking among adults:

United States, 1998. MMWR Morbid

Mortal Wkly Rep 2000;49:881-4.

6. World Bank. Chapter 1, global

trends in tobacco use. In: Curbing

the epidemic: governments and the

economics of tobacco control.

Washington, DC: The World Bank,

1999:13.

7. Bates C, Jarvis M, Connolly G.

Tobacco additives: cigarette

engineering and nicotine addiction,

July 14, 1999.

(www.ash.org.uk/html/regulation/ht

ml/additives.html)

8. Peto, R., Lopez, A. D., Boreham, J.

et al. Mortality from smoking

worldwide. British Medical Bulletin

1996; 52:12–21.

9. Allard, R., Johnson, N., Sardella, A.

et al. Tobacco and oral diseases:

Report of EU Working

Group.Journal of the Irish Dental

Association 1999; 46:12–23.

10. Cogliano V, Straif K, Baab R,

Grosse Y, Secretan B, Ghissassi F E.

Smokeless tobacco and tobacco-

related nitrosamines. The Lancet

Oncology 2004; 5:708.

[Type text]

78



11. Christen AG. Helping patients quit

smoking: lessons learned in the

trenches. Quintessence Int

1998;29:253-9.

12. Christen AG. The clinical effects of

tobacco on oral tissue. J Am Dent

Assoc 1970;81:1378-82.

13. Centers for Disease Control and

Prevention, National Center for

Chronic Disease Prevention and

Health Promotion, Office on

Smoking and Health. Best practices

for Tobacco Cessation: An Essential

Component For Global Public Health

Soni S Dental Imapct vol. 7, Issue 1,

June 2015 comprehensive tobacco

control programs. Atlanta, GA: U.S.

Department of Health and Human

Services, August 1999.

14. Barker GJ, Williams KB. Tobacco

use cessation activities in U.S. dental

and dental hygiene student clinics. J

Dent Educ 1999;63:828-38.

15. McGinnis JM, Foege WH. Actual

causes of death in the United States.

JAMA 1993;270(18):2207-12.

16. Ayanian JZ, Cleary PD. Perceived

risks of heart disease and cancer

among cigarette smokers. JAMA

1999;281:1019-21.

17. West, R., McNeil, A., Raw, M.

Smokeless tobacco cessation

guidelines for health professionals

inEngland. British Dental Journal

2004; 196:611–7.

18. John, J. H., Thomas, D., Richards, D.

Smoking cessation interventions in

the Oxford region:Changes in

dentists’ attitudes and reported

practices 1996–2001. British Dental

Journal 2003;195:270–5.

19. Johnson, N. W., Lowe, J. C.,

Warnakulasuriya, K. A. A. S.

Tobacco cessation activities of UK

dentists in primary care: Signs of

improvement. British Dental Journal

2006; 200:85–9.

20. Christen AG. The dentist’s role in

helping patients to stop smoking. J

Am Dent Assoc 1970;81:1146-52.

21. Christen AG, Cooper KH. Strategic

withdrawal from cigarette smoking.

CA Cancer J Clin 1979;29:96-107.

22. Christen AG, Christen JA, Klein JA.

Nicotine withdrawal therapy in

dental practice: cessation strategies.

Health Values 1993;17:59-68.

23. Fiore MC, Bailey WC, Cohen SJ, et

al. Smoking cessation: clinical

practice guideline No. 18. AHCPR

Publ No. 96-0692. Rockville, MD:

[Type text]

79



U.S. Department of Health and

Human Services, Public Health

Service, Agency for Health Care

Policy and Research, Centers for

Disease Control and Prevention,

April 1996.

24. Fiore MC, Bailey WC, Cohen SJ, et

al. Treating tobacco use and

dependence. clinical practice

guideline. AHRQ Publ No. 00-0032.

Rockville, MD: U.S. Department of

Health and Human Services, Public

Health Service, Agency for

Healthcare Research and Quality,

June 2000.

25. Olson BL, McDonald JL, Gleason

MJ, et al. Comparison of various

salivary parameters in smokers

before and after the use of a nicotine-

containing chewing gum. J Dent Res

1985;64:826-30.

26. Ciancio SG, ed. Section II. Drugs

used in medicine: treatment and

pharmacological considerations for

dental patients receiving medical

care. In: ADA guide to dental

therapeutics. 2nd

ed. Chicago: ADA

Publishing, 2000:569-81.

27. Anderson NB. Integrating behavioral

and social science research at NIH.

Acad Med 1995;70:290-304.

28. Christen AG, Beiswanger BB,

Mallatt ME, et al. Effects of nicotine

containing chewing gum on oral soft

and hard tissues: a clinical study.

Oral Surg Oral Med Oral Path

1985;59:37-42.

29. Shadel WG, Shiffman S, Niaura R,

Nichter M, Abrams DB. Current

models of nicotine dependence: what

is known and what is needed to

advance understanding of tobacco

etiology among youth. Drug Alcohol

Depend 2000;59(Suppl 1):S9-S21.

30. Miller W.R, Rollnick S.

Motivational Interviewing: Preparing

People for Change, Second

Edition.The Guilford Press, 2002.

31. Meyer C, Ulbricht S, Baumeister S,

Schumann A, Rüge J, Bischof G.et

al. Proactive interventions for

smoking cessation in general medical

practices: a quasi-randomized

controlled trial to examine the

efficacy of computer tailored letters

and physician-delivered brief advice.

Addiction 2008; 103: 294–304.

32. Borrelli B, Hogan J.W, Bock B,

Pinto B, Roberts M, Marcus B,

Predictors of quitting and dropout

among women in a clinic-based

smoking cessation program.

[Type text]

80



Psychology of Addictive Behaviours.

Vol 16(1), Mar 2002,22-7.

33. West, R., McNeil, A., Raw, M.

Smoking cessation guidelines for

health professionals: An

update.Thorax 2000; 55:987–99.

34. Jonson GK, Hill M: Cigarette

smoking and the periodontal patient,

J Periodontol 75:196,2004.

35. Cooper TM, Clayton RR. Nicotine

reduction therapy and relapse

prevention for heavy smokers: a 3-

year followup. J Am Dent Assoc

1990;120(Supp):32-6.

36. Christen AG, Jay SJ, Christen JA.

Treating highly dependent smokers

with nicotine gum and patches.

Indiana Med 1996;89:169-74.

37. Transdermal Nicotine Study Group.

Transdermal nicotine for smoking

cessation: six-month results from

two multicenter controlled clinical

trials. JAMA 1991;266:3133-8.

38. National Institute for Health and

Clinical Excellence. Guidance on the

Use of Nicotine Replacement

Therapy (NRT) and Bupropion for

Smoking Cessation. London: NICE,

2002.

39. Christen AG, Christen JA. The

prescription of transdermal nicotine

patches for tobacco- using dental

patients: current status in Indiana. J

Indiana Dent Assoc 1992;71:12-8.

40. Centers for Disease Control and

Prevention. Use of FDAapproved

pharmacologic treatments for

tobacco dependence—United States,

1984-1998. MMWR Morb Mortal

Wkly Rep 2000;49:665-8.

41. Anderson, P. and J.R. Hughes.

"Policy Interventions to Reduce the

Harm from Smoking." Addiction

(2000) 95:9-11.

42. Christen AG, Christen JA.

Smokeless tobacco: intervention

techniques for the dental

professional. Continuing education

course. Dent Assist 1996;65:1-19.

43. Taylor, S.M., et. al. "Community

Intervention Trial for Smoking

Cessation (COMMIT): Changes in

Community Attitudes Toward

Cigarette Smoking." Health

Education Research (1998) 13:109-

122.

44. Abrams BD. Transdisciplinary

paradigms for tobacco prevention

research. Nicotine Tob Res

1999;1:S15-S23.

45. World Health Organization.

International conference on global

[Type text]

81



tobacco control law: towards a WHO

framework convention on tobacco

control, at New Delhi, India, 7-9

January 2002.

46. Jones RB. Tobacco or oral health:

past progress, impending challenge. J

Am Dent Assoc 2000;131:1130

82

REVIEW ARTICLE


MINIMAL INVASIVE DENTISTRY : A REVIEW

Dr. Vanisha Mehta 1,Dr. Vikram Singh


2, Dr.Prajakta Joshi

1

1Post Graduate Student ,

2Senior Lecturer


INTRODUCTION

Preservation of a healthy set of natural teeth

for each patient should be the objective of

every dentist. All work in the health field is

aimed basically at conservation of the

human body and its function. The surgeon is

so conservative that loss of even a small part

of a finger or toe is considered a tragedy.

Likewise Miles Markley, one of eminent

leaders in preventive dentistry, summarized

the contemporary concept in the treatment of

dental caries: that loss of even a part of a

human tooth should be considered “a serious

injury,” and that dentistry’s goal today

should be is to preserve the healthy and what

is natural for tooth structures and tissues .[1]

Minimal invasive dentistry is a “concept that

can embrace all aspects of this profession.

The common delineator is the tissue

preservation, mostly by preventing disease

ABSTRACT:

Advancement in instrumentation, materials & technique have brought the transition

from G.V. Black’s "Extension for prevention" to "Prevention of the extension"

approach in caries management. The concept of "minimally invasive dentistry" can

be defined as to preserve the maximum healthy dental structure. It focuses on

prevention, remineralization & minimal dentist intervention. The minimal loss of

tooth structure is recommended in this type of dentistry. This paper gives light on

describing minimally invasive dentistry from a conceptual perspective, relating to

goals, objectives, principles, clinical caries diagnosis, restorative intervention

threshold and operative procedures.

KEY WORDS: Remineralisation, Minimal invasive dentistry, Ozone. Lasers

83

MINIMAL INVASIVE DENTISTRY : A REVIEW Mehta V et al


from occurring and intercepting its further

progress, but also removing and replacing it

as little tissue loss as possible”.

DEFINITION

The World Congress of MID defines

minimally invasive dentistry as those

techniques, which respect health, function

and esthetics of oral tissue by preventing

disease from occurring, or intercepting its

progress with minimal tissue loss (Nový and

Fuller 2008).

Some authors have defined MID as the

maximal preservation of healthy dental

structures. [2]

GOALS OF MINIMAL

INTERVENTION

1. Reduction in cariogenic bacteria.

2.Minimum surgical intervention of

cavitated lesion.

3. Remineralization of early lesions

4.Repair rather than replacement of

defective restorations

6. Prevention of caries

OBJECTIVES INCLUDE

The four core principles of MID can be

considered to be:

1 Recognition: Early identification and

assessment of potential caries risk factors

through their lifestyle analysis, salivary flow

testing and using plaque diagnostic tests.

2 Reduction: To eliminate or minimize

caries risk factors by altering lifestyle, diet,

habits and increasing the pH of the oral

environment.

3 Regeneration: To arrest and reverse

incipient lesions, using appropriate topical

agents including fluorides.

4 Repair: When cavitation is present and

surgical intervention is required,

conservative caries removal is carried out to

maximize the repair quality of the tooth and

retain the tooth structure.

It has been known for decades

that dental caries is a communicable,

infectious disease caused by dental plaque,

an oral biofilm, and by exposure to

fermentable carbohydrates. Plaque bacteria

produce lactic acid in the presence of

fermentable carbohydrates. This acid

dissolves the calcified component of dental

hard tissues, leading to infection and

progressive loss of tooth structure, pulpal

disease and eventual tooth loss. [3]

Research is ongoing to improve

methods of early caries detection to allow us

to fully implement new approaches to the

management of dental caries. In addition,

84



new caries management protocols have been

developed that differentiate between people

with different levels of caries risk.

Therefore, all restorative procedures must be

carried out only in conjunction with well

understood preventive techniques and

patienteducation.

PRINCIPLES OF MINIMAL

INTERVENTION ARE BASED ON

1. Disease risk assessment & early caries

diagnosis

2. The classification of caries depth and

progression using radiographs

3. The reduction of cariogenic bacteria, to

decrease the risk of further demineralization

and cavitated.

4. The arresting of the active lesions

5. The repair is done rather than replacement

of defective restorations

6. Assessing disease management outcomes

at pre established intervals.

7. The remineralization and monitoring of

non cavitated arrested lesions

8. The placement of restorations in teeth

with cavitated lesions using minimal cavity

designs

STRACT

FigurFigure1: Shows the Etiology of Caries

Figure 2: The Caries Balance: Pathologic

factors versus protective factors. If the caries

balance is heavily weighted in pathogenic

factors, demineralization will prevail and

eventually result in visible changes to teeth.

The earliest visible signs of enamel

demineralization appear as white spots, and

later brown spots, in the enamel. The enamel

surface with white- and brown- spot

lesions.[4]

85



MATERIALS COMMONLY USED IN MID

GIC

RMGIC

Lamination

Advantages - Fluoride release

- Adhesion to tooth by

ion exchange

Improved esthetics The GIC is placed

first because of its

adhesion to dentin

and fluoride release.

Resin-based

composite then is

laminated over the

GIC for the purpose

of improved occlusal

wear or esthetics.

Disadvantages Technique sensitive

- Poor strength

- Improved esthetics

Polymerization

shrinkage

- Low wear resistance

RECENTLY USED TECHNIQUES:

Techniques Method Indications Contraindications

Air abrasion Use stream of air

combine with

superfine abrasive

powder (Aluminium

oxide) to remove

tooth structure.

- Small class I & V

preparation

- Not used in allergic,

asthmatic &medically

compromised patient.

Lasers - Erbium, yttrium- - Based on wavelengths Not used when there is risk

86



aluminium garnet

LASER to cut dental

hardtissue

some are used to cut

hard tissue & others cut

soft tissue without

touching the healthy

tissue

of pulp exposure as amount

of heat may damage pulp

tissue

Chemo mechanical

agent

- Caridex, Carisolv,

papacarie are various

Agents.Used as a

chemical agent

assisted by an

atraumatic mechanical

force to remove

soft carious structure

=Can be used in

anxious uncooperative

& medically

compromised patient

Caridex is time taking &

costly so not indicated in

poor people.

Pit & fissure sealants Fluoride releasing

sealants are most

commonly used

-Newly erupted

primary molars &

permanent bicuspids &

molars

-Stained pits & fissure

with minimum

decalcification

Individual with no previous

caries experience

- Wide & self-cleansable

pit &fissure

- Pits & fissures that are

caries freefor 4 yrs or

longer

- Partially erupted teeth

Some other disinfectants in arresting dental

caries:

OZONE

Ozone (O3) is a powerful oxidizing agent

which neutralizes acids and its effects on

cell structures, metabolism and

87



microorganisms are well-documented.

Researches has shown that ozone disrupts

the cell walls of microorganisms (bacteria

and viruses) within seconds, leading to

immediate functional cessation. This rapid

effect has clinical significance, as the

potential for microbial resistance to this

treatment modality is insignificant. In view

of its powerful oxidizing properties. Ozone

can also attack many bio-molecules such as

the cysteine, methionine and the histidine

residues of proteins and can make change in

the surface ecology of the carious lesion.

Remineralization from salivary ions occurs

readily, due to the surface changes on the

exposed dentinal tubules. It is a naturally

produced by the photo dissociation of

molecular O2 into activated oxygen atoms,

which then react with further oxygen

molecules. This transient radical anion

rapidly becomes protonated, generating

bicarbonates, which, in turn, decomposes to

an even more powerful oxidant, the

hydroxyl radical (OH ions).

PHOTO-ACTIVATED DISINFECTION

is a method of disinfecting or sterilizing a

site (tissues, wounds and lesions of the oral

cavity) by topically applying a

photosensitizing agent (a dye) and removing

the site with laser light at a wavelength

absorbed by the photosensitizing agent.

Destruction of the microbes occurs without

damage to other tissues at this site.[4]

BENEFITS OF MI

The benefit for patients from MI lies in

better oral health through disease healing,

not merely symptom relief. Furthermore, MI

may assist in reducing widespread patient

dental anxieties, which are usually caused

by conventional, highly invasive dental

procedure.[5]

CONCLUSION

An astute dentist should apply the

concepts of MID for the conservative

management of dental caries and

simultaneously offer patients a friendlier and

health orientated treatment option for the

victorious management.

REFERENCES:

1. Kinch C. Minimally invasive

dentistry. Journal of American

Dental association. 2003; 13(4): 87-

95.

2. Gutmann. Minimally invasive

dentistry .Journal of Conservative

Dentistry.2013;16 (4):282-3.

3. Walsh L, Brostek AM. Minimal

Intervention Dentistry principles and

objectives. Research Centre for Oral

Health Sciences: 1-33.

88



4. Brostek A, Bochenek A,Walsh,L.

Minimally invasive operative

technique using high tech dentistry.

Dental practice .2006; 107-8.

5. Gujjar KR, Sumra N. Minimally

Invasive Dentistry - A Review.

International Journal of Clinical

Preventive Dentistry.2013; 9(2):109-

120.

6. Houpt M, Fukus A, Eidelman E.The

preventive resin (composite

resin/sealant) restoration: nine-year

results. Quitessence Int 1994; 25:

155-9.

7. Smales RJ, Yip HK. The atraumatic

restorative treatment (ART)

approach for the management of

dental caries. Quintessence Int 2002;

33: 427-32.

8. Munshi AK, Hegde AM, Shetty PK.

Clinical evaluation of carisolv in the

chemico-mechanical removal of

carious dentin. J Clin Pediatr Dent

2001; 26: 49-54.

9. Walsh LJ. The current status of laser

applications in dentistry. Aust Dent J

2003; 48:146-55.

10. Berry EA 3rd, Eakle WS, Summitt

JB. Air abrasion: an old technique

reborn. Compend Comm Educ Dent

1999;20: 751-4

11. Banerjee A, Watson TF, Kidd EA.

Dentine caries excavation; a review

of current clinical techniques. Br

Dent J 2000; 188: 476-82.

12. Colston BW Jr, Everett MJ, Sathyam

US, DaSilva LB, Otis LL. Imaging

of the oral cavity using optical

coherence tomography. Monogr Oral

Sci 2000;17:32-55.

13. Pitts NB. Risk assessment and caries

prediction. J Dent Educ

1998;62(10):762-70.

14. Pitts NB, Rimmer PA. An in vivo

comparison of radiographic and

directly assessed clinical caries status

of posterior approximal surfaces in

primary and permanent teeth. Caries

Res 1992;26:146-52.

15. Mount GJ, Hume WR. A revised

classification of carious lesions by

site and size. Quintessence Int

1997;28:301-3.

16. Benn DK, Meltzer MI. Will modern

caries management reduce

restorations in dental practice? J Am

Coll Dent 1996;63(3):39-44.

17. Rothwell M, Anstice HM, Pearson

GJ. The uptake and release of

fluoride by ion-leaching cements

after exposure to toothpaste. J Dent

1998;26(7):591-7.

89



18. Abdalla AI, Alhadainy HA, Garcia-

Godoy F. Clinical evaluation of glass

ionomers and compomers in Class V

carious lesions. Am J Dent

1997:10(1):18-20.

19. Pereira AC, Pardi V, Basting RT, et

al. Clinical evaluation of glass

ionomers used as fissure sealants:

24-month results. ASDC J Dent

Child 2001:68(3):168-74, 150.

20. de Araujo MA, de Araujo RM,

Marsilio AL. A retrospective look as

esthetic resin composite and glass-

ionomer class III restorations: a 2-

year clinical evaluation.

Quintessence Int 1998;29(2):87-93.

21. Van Dijken JW. Longevity of new

hybrid restorative materials in class

III cavities. Eur J Oral Sci

1999;107(3):215-9.

22. Jang KT, García-Godoy F, Donly

KJ, Segura A. Remineralizing effects

of glass ionomer restorations on

adjacent interproximal caries. ASDC

J Dent Child 2001;68(2):125-8, 142.

23. Croll TP, Bar-Zion Y, Segura A,

Donly KJ. Clinical performance of

resin-modified glass ionomer cement

restorations in primary teeth: a

retrospective evaluation. JADA

2001;132(8):1110-6.

24. Toledano M, Perdigao J, Osorio R,

Osorio E. Effect of dentin

deproteinization on microleakage of

Class V composite restorations. Oper

Dent 2000; 25(6):497-504.

25. Manhart J, Chen HY, Mehl A,

Weber K, Hickel R. Marginal quality

and microleakage of adhesive class

V restorations. J Dent

2001;29(2):123-30.

26. Wendt LK, Koch G, Birkhed D.

Replacements of restorations in the

primary and young permanent

dentition. Swed Dent J 1998;

22(4):149-55.

27. Roberts HW, Charlton DG,

Murchison DF. Repair of non-

carious amalgam margin defects.

Oper Dent 2001;26 :273-6.

28. Anusavice KJ, Benn DK. Is it time to

change state and regional dental

licensure board exams in response to

evidence from caries research? Crit

Rev Oral Biol Med 2001;12(5):368-

72.

29. Reyto R. Lasers and air abrasion.

New modalities for tooth

preparation.Dent Clin North Am

2001;45(1):189-206.

30. Hamilton JC, Dennison JB, Stoffers

KW, Welch KB. A clinical

90



evaluation of air-abrasion treatment

of questionable carious lesions: a 12-

month report. JADA 2001;132 :762-

9.

31. Friedman MJ, Mora AF, Schmidt R.

Microscope-assisted precision

dentistry. Compendium

1999;20(8):723-37.

91

REVIEW ARTICLE


KEEP CARIES AWAY: GET IMMUNIZED

Dr Prajakta Joshi 1, Dr. Vikram Singh


2, Dr. Vanisha Mehta

1


2Senior Lecturer


5Senior Lecturer, Department Of Pedodontics

6Post Graduate Student, Department Of Pedodontics

INTRODUCTION

Dental caries is the most common disease

that is prevalent among developed,

developing, and underdeveloped countries

affecting the adults as well as children.[1]

It is an irreversible microbial disease of the

calcified tissues of the teeth, which is

characterized by demineralization of the

inorganic portion and destruction of the

organic substance of the tooth, which often

leads to cavitations.[2] Dental caries forms

through a complex interaction over time

between the various acid-producing

bacteria and the fermentable

carbohydrates, and many other host factors

which includes teeth and saliva.[3] A wide

group of microorganisms that are isolated

from the carious lesions are S.mutans,

Lactobacillus acidophilus (L.acidophilus),

Lactobacillus fermentum (L.fermentum),

Actinomyces viscosus (A.viscosus) which

are found to be the main pathogenic

species involved in the initiation and

progression of carious lesions.[4] These

cariogenic bacteria are capable of

producing acids by fermenting the

carbohydrates present in the diet and S.

mutans is the most prevalent species

ABSTRACT:

Dental caries is one of the most common microbial diseases of mankind. Cariogenic

micro-organisms enters the biofilm early phase of life and subsequently develops,

under favorable environmental conditions, to cause disease. Adaptive host defences

are aroused by these infections and are expressed in the saliva and gingival

crevicular fluid. This paper review will focus on methods by which the mucosal host

defences can be induced by immunization to interfere with dental caries caused by

Streptococci mutans (S.mutans) and the various recent progresses in the

development of mucosal adjuvants and delivery systems for dental caries vaccines.

KEY WORDS: Dental Caries, Streptococcus mutans (S.mutans), Caries Vaccine,

Immunization

92

KEEP CARIES AWAY: GET IMMUNIZED Joshi P et al


among all and has been implicated as a

causative organism of dental caries.[5]

Hence, most of the treatments are now

aimed at either the elimination of this

bacterium or suppression or inhibition of

its virulence. Currently, contemporary

researches are aimed at evolving a potent

and significantly effective caries vaccine

to prevent dental caries that is well suited

for public health applications.[1]

MOLECULAR PATHOGENESIS OF

THE DISEASE

The molecular pathogenesis of S.mutans

appears to involve various stages each of

which may offer target sites for

immunological intervention.[6]

Acidogenic streptococci require the hard

surfaces for their sustained colonization

and accumulation. The initial attachment

to the tooth is achieved by the interaction

of bacterial proteins with lectins present in

the dental pellicle covering the tooth

surface which is a characteristic trait of a

family of streptococcal adhesins, and

referred to as antigen I/II or PAC in

S.mutans, which is demonstrated to attach

to salivary components in experimental

tooth pellicles.[7]

The ultimate pathogenicity of S.mutans

occurs through the erosion of the

hydroxyapatite-like mineral in enamel by

lactic acid which is a bacterial metabolic

end-product. But, significantly destructive

concentrations of this acid require a

substantial accumulation of these

acidogenic streptococci in dental plaque

and by the activity of extracellular

glucosyltransferases (GTF) which are

constitutively secreted by S.mutans, this

accumulation process is initiated. GTFs

synthesize various forms of high-

molecular- weight branched extracellular

glucans, in the presence of sucrose.[8] The

most closely associated with microbial

pathogenicity are the GTFs that synthesize

insoluble forms of glucan (S. mutans GTF-

B & GTF-C). Through the series of

interactions with the bacterial cell-

associated glucan-binding proteins (GBP)

and several such glucan- binding proteins

these glucose polymers provide a

scaffolding for the aggregation of mutans

and other oral streptococci have been

demonstrated in S. mutans and S. sobrinus.

GTFs also contain glucan-binding domains

which permit binding to glucans and these

interactions of glucans with cell-associated

glucan-binding domains of GTFs and

GBPs combine to a cause extensive

accumulation of S.mutans in the dental

biofilm.[9]

The next phase of pathogenesis results

from the several metabolic activities of

these accumulated masses of S.mutans and

the other accumulated micro-organisms. S.

93



mutans are the most potent producers of

lactic acid in these accumulations although

other less potent that is “low pH bacteria”

may also contribute.[10]

Dental caries then progresses, because of

the resulting increase in lactic acid

synthesis that cannot be sufficiently

buffered by saliva to prevent enamel

dissolution and to inhibit the caries

activity.[8]

EFFECTIVE MOLECULAR

TARGETS FOR CARIES VACCINE

Various stages in the molecular

pathogenesis of dental caries are

susceptible to immune intervention.

Clearance of the micro-organisms from the

oral cavity can be done by antibody-

mediated aggregation in the salivary phase,

prior to their colonization.[1] Antibodies

could also block the receptors which are

necessary for colonization (adhesins) or

their accumulation (glucan-binding

domains of GBPs and GTF), or to

inactivate GTF enzymes responsible for

glucan formation. The antimicrobial

activity of salivary IgA antibody may be

enhanced, increased or redirected by

synergism with the innate components of

immunity, such as mucin or lactoferrin.[8]

The present review will concentrate on

adhesins, GTFs, and GBPs and Dextranase

as vaccine targets, since most of the recent

experimental have exploited these

components for vaccine development.

Adhesions

Adhesins are generally purified from the

two principal human pathogens.[11]

S.mutans (variously identified as antigen

I/II, PAc, or P1) and S.sobrinus (SpaA or

PAg), but despite their homology, the two

mutans streptococcal adhesions appears to

bind with separate components in the

pellicle.[12] This protein is composed of a

single polypeptide chain of approximately

1600 residues in length.[13] S. mutans Ag

I/II contains an alanine-rich tandem of

repeating region in the N-terminal third,

and a proline-rich repeat region in the

centre of the molecule associated with the

adhesin activity of Ag I/II. Immunological

approaches support the adhesin-related

function of the AgI/II family of proteins

and their repeating regions with abundant

in vitro and in vivo evidence which states

that antibody with specificity for S. mutans

AgI/II or S. sobrinus SpaA interferes with

bacterial adherence and subsequent dental

caries. Antibody directed to the intact

antigen I/II molecule or to its salivary-

binding domain blocks the adherence of S.

mutans to saliva-coated hydroxyapatite.[7]

Furthermore, several other immunization

approaches have shown that active

immunization with intact antigen I/II or

passive immunization with the monoclonal

94



or transgenic antibody to putative salivary-

binding domain epitopes within this

component can even protect rodents,

primates, or humans from dental caries

caused by S. mutans.[14] Hence from

these experiments, protection could

conceivably occur by antibody blockade of

initial colonization events or antibody-

mediated agglutination and clearing of

adhesion bearing bacteria from the saliva.

Glucosyltransferase (GTF)

S. mutans and S. sobrinus each synthesize

several forms of glucosyltransferases. The

sequences of these enzymes vary from

1400 to nearly 1600 amino acid residues

and contain considerable sequence

homology, despite differences in their

water-solubility and linkages among the

glucans that are synthesized. Genes that

are responsible for glucan synthesis in S.

mutans are gtfB which synthesizes an a-

1,3-linked insoluble glucan,[15] gtfC

which synthesizes glucan with both a- 1,3

and a-1,6 linkages[16], and gtfD which

synthesizes a soluble a-1,6-linked

glucan.[17] In the same way, the products

of gtfI and gtfS genes of S. sobrinus

synthesize insoluble and soluble glucan

products, respectively. Induction of SIgA

antibody in humans by oral or topical GTF

administration is accompanied by the

interference with the accumulation of

indigenous S.mutans after dental

prophylaxis and passive administration of

antibody to GTF in the diet can protect rats

from experimental dental caries.[18] Thus,

the presence of antibody to

glucosyltransferase in the oral cavity

before the infection can significantly

influence the disease outcome, presumably

by interference with the functional

activities of the enzyme.

Glucan – binding protein (GBP)

The ability of mutans streptococci to bind

to glucans is mediated, at least in part, by

cell-wall-associated glucan-binding

proteins (Gbp). Many other proteins with

glucan binding properties have been

evident in S.mutans and S.sobrinus.[19] S.

mutans secretes at least three different

proteins with glucan-binding activity:

GbpA, GbpB and GbpC. GbpA has a

deduced sequence of 563 amino acids with

the molecular weight of 59.0 kDa and that

of GbpB protein is 431 residues long with

a calculated molecular weight of 41.3 kDa

and the third S. mutans non-enzymatic

glucan-binding protein, GpbC, is

composed of 583 amino acids and

calculated molecular weight of 63.5

kDa.[8]

Only GbpB of the three S. mutans glucan-

binding proteins, has been evident to

induce a protective immunity to

experimental dental caries. It can either be

95



achieved by subcutaneous injection in the

salivary gland region[20] or by mucosal

application through the intranasal

route.[21] Saliva of young children often

contain IgA antibody to GbpB, which

indicates that initial infection with S.

mutans can led to natural immune

response.[22]

Dextranase

Dextranase, an important enzyme

produced by S. mutans,that destroys

dextran, an important constituent of early

dental plaque, so that the bacterium can

easily invade dextran- rich early dental

plaque. Dextranase if used as an antigen

can potentially prevent colonization of the

organism in early dental plaque.[23]

Different Routes Of Immunization

Since secretory IgA immunoglobulin

constitutes the major immune component

of major and minor salivary gland

secretions, their mucosal applications are

generally preferred. Evidence shown that

exposure of antigen to mucosally

associated lymphoid tissue in the gut,

nasal, bronchial, or rectal site can give rise

to immune responses not only in the region

of induction, but also in remote locations

and hence given rise to the notion of a

“common mucosal immune system”.[24]

Consequently, several other mucosal

routes have been used to induce protective

immune responses to dental caries vaccine

antigens.

(A) Oral Route

Previous studies relied on the oral

induction of immunity in the gut-

associated lymphoid tissues (GALT) to

elicit the protective salivary IgA antibody

responses where the antigen was applied

by oral feeding, gastric intubation, or in

vaccine-containing capsules or liposomes.

Various animal trials conducted on

germfree rats by administering them with

killed S. mutans in drinking water resulted

in significant reduction of caries related to

increased level of salivary IgA

antibodies.[7] Oral immunization of 7

adult volunteers with an enteric coated

capsule containing 500 micrograms of

GTF from S. mutans resulted in elevating

salivary IgA antibodies to the antigen

preparation.[8] Although the oral route

was not found to be ideal for reasons

including the detrimental effects of

stomach acidity on antigen, or because

inductive sites were relatively at distance,

experiments with this route established

that induction of mucosal immune

response alone was sufficient to change the

course of S.mutans infection and disease in

animal models.[25]

(B) Intranasal Route

More recently, attempts have been made to

induce protective immunity in mucosal

96



inductive sites that are in nearer

anatomical relationship to the oral cavity

so intranasal installation of

antigen, targets the Nasal-Associated

Lymphoid Tissue (NALT) used to induce

immunity.[26] Protection could be

demonstrated with S. mutans AgI/II, a 19-

mer sequence within the SBR, the glucan-

binding domain of S. mutans GTF-B, S.

mutans GbpB and fimbrial preparations

from S. mutans with antigen alone or

combined with mucosal adjuvants.[8]

(C) Tonsillar Route

Great interest has been aroused due to the

ability of tonsillar application to induce

immune responses in the oral cavity as

tonsillar tissue contains the elements of

immune induction of secretory IgA

responses although IgG, response

characteristics are dominant in this

tissue.[27,28] The palatine tonsils, and

especially the nasopharyngeal tonsils, are

suggested to contribute for the percursor

cells to migrate to mucosal effector sites,

such as the salivary glands.[29]

(D) Minor Salivary Glands

Lips, cheeks and soft palate are the major

sites for the location of minor salivary

glands and have been suggested as

potential routes for the mucosal induction

of salivary immune responses, given their

short, broad secretory ducts which

facilitate retrograde access of bacteria and

their products,[30] and given the lymphatic

tissue aggregates which are often found to

be associated with these ducts. In these

experiments, those who received labial

application of GTF showed significantly

lower concentrations of indigenous

S.mutans/total streptococcal flora in their

whole saliva during the six-week period

follow-up after a dental prophylaxis,

compared with a placebo group.[31]

(E) Rectal Route

The colo-rectal region generally is an

inductive location for mucosal immune

responses in humans as this site has the

highest concentration of lymphoid follicles

in the lower intestinal tract. Various

preliminary studies have concluded that

this route could also be used to induce

salivary IgA responses to S.mutans

antigens such as GTF. One could therefore

look forward for the use of vaccine

suppositories as one alternative for

children in whom respiratory ailments

preclude intranasal application of

vaccine.[32]

(F) Systemic Route

Serum IgA, IgG and IgM antibodies were

produced as a result of successful

subcutaneous administration of S. mutans

in monkeys. The antibodies find their way

into the oral cavity via the gingival

crevicular fluid and are protective against

dental caries. Studies have shown that IgG

antibodies are well maintained at high titre

while IgM antibodies progressively fall

97



and IgA antibodies increases slowly in

titre. The development of serum IgG

antibodies takes place within months of

immunization, reaching a tire of upto

1:1280.[33]

(G) Active Gingivo-Salivary Route

To minimize the potential side effects

associated with other routes of vaccine

administration, and to localize the immune

response, gingival crevicular fluid has

been used as the route of

administration.[33]

ADJUVANTS AND DELIVERY

SYSTEM FOR THE VACCINE

Clinical trials have been performed to

examine the protective effect of active

immunization with dental caries vaccines.

Mucosal application of soluble protein or

peptide antigens by themselves rarely

results in sustained IgA responses.

Considerable effort, therefore, has been

expended to develop immunomodulators

(adjuvants) and delivery systems that

enhance mucosal responses, including

responses to dental caries vaccines.

Various new approaches have been tried in

order to overcome the existing

disadvantages.

Synthetic peptides

Synthetic peptide approaches have shown

the alanine-rich repeat region of Ag I/II to

be immunogenic and to induce protective

immunity. The synthetic peptides give

antibodies not only in the gingival

crevicular fluid but also in the saliva. The

synthetic peptide used is derived from the

GTF enzyme.[34]

Coupling with Cholera and E. coli toxin

subunits

It has been found that coupling of the

protein with non-toxin unit of the Cholera

Toxin (CT) was also effective in

suppressing the colonization of

S.mutans.[34] CT is a powerful mucosal

immune-adjuvant which is frequently used

to enhance the induction of mucosal

immunity to

a variety of bacterial and viral pathogens

in animal systems. Mucosal application of

soluble protein or peptide antigen alone

very rarely results in elevated or sustained

IgA responses. However, addition of small

amounts of CT or the closely related E.coli

heat-labile enterotoxins (LT) can

potentially enhance the mucosal immune

responses to intragastrically or intranasally

applied streptococcal antigens or to

peptides that are derived from these

antigens.[8]

Recombinant vaccines

Recombinant approaches potentiate the

expression of larger portions of functional

domains than can be accommodated by

synthetic peptides. The virulent strains of

Salmonella are potentially effective

vaccine vector so that fusion using

recombinant techniques has been used.

Salmonella vaccine was effective in

98



inducing protection against S. sobrinus in

rats and that prolonged persistence of

recombinant S. typhimurium in the Peyer’s

patches or spleens was not required for

induction of this protective immune

response.[35]

Liposomes

These have been used in the delivery of

several, particularly anticancer, drugs so as

to effectively target the cells to where it

should reach. These liposomes are closed

vesicles with bilayered phospholipid

membrane. Liposomes are supposed to

improve mucosal immunity by facilitating

M cell uptake and delivery of antigen to

lymphoid elements of inductive tissue. The

efficacy using liposomes has been found to

increase two fold in a rat model. In

humans increased IgA antibodies have

been found.[8,34]

Microcapsules and microparticles

Combinations of antigen in or on various

types of particles have been used in

attempts to enhance mucosal immune

responses. Microspheres and

microcapsules which are made of poly

lactide-co-glycolide (PLGA) have been

generally used as local delivery systems

because of their characteristic ability to

control the rate of release, evade pre-

existent various antibody clearance

mechanisms, and degrade or decrease

slowly without eliciting an inflammatory

response to the polymer. Oral

immunization with these kinds of

microspheres effectively delivered the

target sites and released the vaccine in the

gut associated lympohoid tissue as defined

by their ability to induce a disseminated

mucosal IgA anti-toxin antibody

response.[36]

Conjugate vaccines

Another vaccine approach which can

intervent more than one aspect of mutans

streptococcal molecular pathogenesis is the

chemical conjugation of the functionally

associated protein/peptide components

with bacterial polysaccharides. More to the

value of multiple targets within the vaccine

is the conjugation of protein with

polysaccharide which enhances the

immunogenicity of the T-cell independent

polysaccharide entity.[8]

PAST, PRESENT AND FUTURE

HUMAN APPLICATION

(A) Active Immunization

Few clinical trials have been performed till

now to examine the protective effect of

active immunization with dental caries

vaccines containing definite antigens.

However, several studies have shown that

mucosal exposure to immunization

through vaccines with glucosyltransferases

from S.mutans or S. sobrinus can greatly

influence the formation of salivary IgA

antibody, at modest levels. Childers and

co-workers (1994) orally immunized

adults using the enteric-coated capsules

99



which are filled with crude S.mutans GS-5

GTF antigen preparations in

liposomes.[37] Parotid salivary IgA

antibody responses were induced in five of

seven subjects. Similarly, nasal

immunization with dehydrated liposomes

containing the GTF preparation induced a

significant IgA1 antibody response in

nasal washes. Parotid salivary antibody

levels to GTF were of lower

magnitude.[38] In earlier studies, this

group showed that oral administration of

capsules containing the purified serotype

carbohydrate antigen of S.mutans in

liposomes gave rise to minimal but

detectable levels of salivary antibody.

Smith and Taubman (1990) reported that

mucosal immunization with GTF can also

influence the re-emergence of mutans

streptococci in young adults after a dental

prophylaxis.[31]Levels of parotid salivary

IgA antibody increased after an oral

immunization with S.sobrinus GTF

through enteric capsules, administered

with aluminum phosphate. Immunization

by this protocol delayed the re-

accumulation of indigenous oral S.mutans,

compared with a placebo group. Similar

results, as delay in S.mutans re-emergence

was observed after topical administration

of GTF on the lower lip. Although this

procedure did not result in a significant

detectable increase in antibody. So

evidently, these studies support the

hypothesis that the mucosal immunization

with dental caries vaccines could be

protective, especially in children where

S.mutans is not a permanent member of

the dental biofilm till then.[8]

(B) Passive Immunization

Another approach lies in the development

of antibodies that are suitable for passive

oral application against dental caries. This

has a considerable potential advantage in

which it completely avoids any risks that

might arise from active immunization.

Conversely, in the case where there is

absence of any active response on the part

of the recipient, there is no induction of

immunological memory, and even the

administered antibodies can persist in the

mouth for only a few hours at most or up

to 3 days in plaque.[39]

Passive antibody administration has also

been researched and worked on for effects

on indigenous S.mutans. Several

approaches are tried.[1]

Longer-term effects on

indigenous flora were observed

after topical application of

mouse monoclonal IgG or

transgenic plant secretory S-

IgA/G antibody, each with

specificity for Ag I/II.[14]

Researchers are also working

on ways to inject a peptide in

the fruit that blocks the

100



bacterium S.mutans which

causes tooth decay so that

cavities and painful visits to the

dentist could become a thing of

the past. They are trying to find

new ways to deliver the

peptides into the oral cavity

through apples and

strawberries.[34]

Mouth rinses containing bovine

milk or hen egg yolk IgY

antibody to S. mutans cells

which led to modest short-term

decreases in the numbers of

indigenous S.mutans in saliva

or dental plaque.[40]

The latest development in the

field of passive immunization

is the use of transgenic plants

to give the antibodies. The

researchers have developed a

caries vaccine by generating

four transgenic Nicotiana

tabacum plants that expressed a

murine monoclonal antibody

kappa chain also a hybrid

immunoglobulin A-G heavy

chain, a murine joining chain,

and a rabbit secretory

component, respectively. The

vaccine, which is colourless

and tasteless, can be painted

onto the teeth rather than

injected and is the first plant

derived vaccine from GM

plants.[41]

(C) Prospects And Concerns

All vaccines, if properly manufactured and

administered, seem to have no risks. The

most serious risk is that the sera of some

patients with rheumatic fever who show

serological cross-reactivity between heart

tissue antigens and certain antigens from

hemolytic Streptococci. In most of the

developing countries of the world, there

has been a rapid increase in dental caries in

both children and adolescents.[33]

Traditional vaccine therapy shows that

immunization should be induced prior to

infection as the apparent pattern of

S.mutans colonization and the association

of these organisms with disease, would

suggest that immunization for dental caries

should promisingly begin early in the

second year of life for the populations who

is under “normal” risk for infection.[8]

Bacterial colonization of the dental biofilm

generally complete after eruption of all

primary teeth and if possible one can,

through immunization, prevent S.mutans

streptococcal colonization prior to this

time, then the benefit of early

immunization might extend until the

permanent teeth begin to erupt, exposing

new ecological conditions.[1]

Thus a successful vaccination directed

against S. mutans can go a long way in

101



improving the caries status of the

vulnerable populations and serve as a

major public health measure in others.

REFERENCES

1. Gambhir RS, Singh S, Singh G,

Singh R, Nanda T, Kakar H.

Vaccine against dental caries.

Journal of vaccines and

vaccination. 2012;3(2):1-7.

2. Shafer’s text book of oral

pathology. 5th ed.

3. Selwitz RH, Ismail AI, Pitts NB

.Dental caries. 2007;369:51-9.

4. Aas JA, Griffen AL, Dardis SR,

Lee AM, Olsen I, et al.Bacteria of

dental caries in primary and

permanent teeth in children and

young adults. J Clin Microbiol.

2008;46: 1407-17.

5. Mattos-Graner RO, Smith DJ. The

vaccination approach to control

infections leading to dental caries.

Braz J Oral Sci. 2004;3: 595-608.

6. Staat RH, Langley SD, Doyle RJ.

Streptococcus mutans adherence:

presumptive evidence for protein-

mediated attachment followed by

glucan-dependent cellular

accumulation. Infect Immun.

1980;27:675-81.

7. Hajishengallis G, Nikolova E,

Russell MW. Inhibition of

Streptococcus mutans adherence to

saliva-coated hydroxyapatite by

human secretory immunoglobulin

A (S-IgA) antibodies to cell surface

protein antigen I/II: reversal by

IgA1 protease cleavage. Infect

Immun. 1992;60:5057-64

8. Smith DJ. Dental Caries Vaccine:

Prospects and Concerns. Crit Rev

Oral Biol Med 2002.13(4):335-49.

9. Marwah N. Textbook Of Pediatric

Dentistry.3rd

Edition

10. Van Ruyven FO, Lingstrom P, van

Houte J, Kent R. Relationship

among mutans streptococci, “low-

pH” bacteria, and iodophilic

polysaccharide-producing bacteria

in dental plaque and early enamel

caries in humans. J Dent Re.

2000;79:778-84.

11. Russell MW, Lehner T.

Characterization of antigens

extracted from cells and culture

fluids of Streptococcus mutans

serotype c. Arch Oral Biol. 1978;

23:7-15.

12. Gibbons RJ, Cohen L, Hay DI.

Strains of Streptococcus mutans

and Streptococcus sobrinus attach

to different pellicle receptors.

Infect Immun. 1986;52:555-61.

13. Lee SF.,Progulske-Fox A, Bleiweis

AS. Molecular cloning and

expression of a Streptococcus

mutans major surface protein

antigen P1 (I/II) in Escherichia

102



coli. Infect Immun.1988;56:2114-

9.

14. Ma JK, Hikmat BY, Wycoff K,

Vine ND, Chargelegue D, Yu L, et

al.. Characterization of a

recombinant plant monoclonal

secretory antibody and preventive

immunotherapy in humans. Nature

Med. 1998; 4:601-6

15. Shiroza T, Ueda S, Kuramitsu HK.

Sequence analysis of then gtfB

gene from Streptococcus mutans. J

Bacteriol 1987; 169:4263-70

16. Pucci MJ, Jones KR, Kuramitsu

HK, Macrina FL. Molecular

cloning and characterization of the

glucosyltransferase C gene (gtfC)

from Streptococcus mutans LM7.

Infect Immun. 1987;55:2176-82.

17. Honda O, Kato C, Kuramitsu HK.

Nucleotide sequence of the

Streptococcus mutans gtfD gene

encoding the glucosyltransferase- S

enzyme. J Gen Microbiol.

1990;136:2099-105

18. Smith DJ, Taubman MA. Oral

immunization of humans with

Streptococcus sobrinus

glucosyltransferase. Infect

Immun.1987;55:2562-9.

19. Smith DJ, King WF, Wu CD, Shen

BI, Taubman MA . Structural and

antigenic characteristics of

Streptococcus sobrinus glucan

binding proteins. Infect Immu.

1998; 66:5565-9.

20. Smith DJ, Taubman MA.

Experimental immunization of rats

with a Streptococcus mutans 59

kDa glucan binding protein

protects against dental caries.

Infect Immu. 1996;64:3069-73.

21. Smith DJ, Heschel RL, Melvin J,

King WF, Pereira MBB, Taubman

MA. Streptococcus mutans glucan

binding proteins as dental caries

vaccines. In: Mucosal solutions.

Advances in mucosal

immunology.1997;2:367-77.

22. Smith DJ, King WF, Akita H,

Taubman MA (1998a). Association

of salivary IgA antibody and initial

mutans streptococcal infection.

Oral Microbiol Immuno.1998;

13:278-85.

23. Krithika AC, Kandaswamy D,

Krishna VG .Caries Vaccine-1.

Today’s myth. J Indian Assoc

Public Health Dent.2004; 4: 21-5.

24. Mestecky J . Saliva as a

manifestation of the common

mucosal immune system. Ann NY

Acad Sci. 1993;694:184-94.

25. Michalek SM, McGhee JR,

Mestecky J, Arnold RR, Bozzo L.

Ingestion of Streptococcus mutans

induces secretory IgA and caries

103



immunity. Science. 1976;

192:1238-40.

26. Brandtzaeg P, Haneberg B. Role of

nasal-associated lymphoid tissue in

the human mucosal immune

system. Mucosal Immunol Update.

1997;5:4-8.

27. Van Kempen MJ, Rijkers GT, Van

Cauwenberge PB. The immune

response in adenoids and tonsils.

Int Arch Allergy Immunol.

2000;122:8-19.

28. Boyaka PN, Wright PF, Marinaro

M, Kiyono H, Johnson JE,

Gonzales RA, et al.Human

nasopharyngeal-associated

lymphoreticular tissues. Functional

analysis of subepithelial and

intraepithelial B and T cells from

adenoids and tonsils. Am J Pathol.

2000; 157:2023-35.

29. Brandtzaeg P. The B-cell

development in tonsillar lymphoid

follicles. Acta Otolaryngol.

1996;523(6):55-9.

30. Nair PN, Schroeder HE.

Retrograde access of antigens to

the minor salivary glands in the

monkey Macaca fascicularis. Arch

Oral Biol. 1983;28:145-52.

31. Smith DJ, Taubman MA. Effect of

local deposition of antigen on

salivary immune responses and

reaccumulation of mutans

streptococci. J Clin Immunol.

1990;10:273-81.

32. Lam A, Smith D, Barnes L,

Clements JD, Wise D, Taubman

MA. Alternate routes for dental

caries vaccine delivery. J Dent

Res.2001; 80:124.

33. Shivakumar KM, Vidya SK,

Chandu GN. Dental caries vaccine.

Indian J Dent Res. 2009;20: 99-106

34. Tandon S. Textbook of

Pedodontics. (2nd edn), Paras

Publishing, New Delhi.2008

35. Redman TK, Harmon CC, Lallone

RL, Michalek SM. Oral

immunization with recombinant

Salmonella typhimurium

expressing surface protein antigen

A of Streptococcus sobrinus: dose

response and induction of

protective humoral responses in

rats. Infect Immun 63: 2004-11.

36. Russell MW, Hajishengallis G,

Childers NK, Michalek SM.

Secretory immunity in defense

against cariogenic mutans

streptococci. Caries Res.1999 33:

4–15.

37. Childers NK, Zhang SS, Michalek

SM. Oral immunization of humans

with dehydrated liposomes

containing Streptococcus mutans

glucosyltransferase induces

salivary immunoglobulin A2

104



antibody responses. Oral Microbiol

Immunol.1994.9: 146–53.

38. Childers NK, Tong G, Michalek

SM. Nasal immunization of

humans with dehydrated liposomes

containing Streptococcus mutans

antigen. Oral Microbiol Immunol.

1997;12:329-35

39. Russell MW, Childers NK,

Michalek SM, Smith DJ, Taubman

MA. A Caries Vaccine? The state

of the science of immunization

against dental caries Caries Res.

2004;38: 230-35.

40. Filler SJ, Gregory RL, Michalek

SM, Katz J, McGhee JT. Effect of

immune bovine milk on

Streptococcus mutans in human

dental plaque. Arch Oral Biol.

1991;36:41-47.

41. Ma JK, Hiatt A, Hein M, Vine ND,

Wang F, et al.Generation and

assembly of secretory antibodies in

plants. Science. 1995;268: 716-19.

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